tag:blogger.com,1999:blog-87235820745390219482014-12-11T18:15:02.791-05:00My Variables Only Have 6 LettersProgramming in languages older than you are is fun...and now I need to start your IV.Christopherhttp://www.blogger.com/profile/11415988855392944633noreply@blogger.comBlogger85125tag:blogger.com,1999:blog-8723582074539021948.post-48952016929352266392013-02-20T19:56:00.000-05:002013-02-20T19:56:03.770-05:00Challenging Tradition: Better Precordial Lead Placement<i>This post is part of a series presenting challenges to the traditions of EMS.</i><br /><i><br /></i><b>Challenging Tradition: Better Precordial Lead Placement</b><br /><br />Application of the precordial electrodes for a 12-Lead ECG is a process steeped in over 75 years of tradition. Drs. Wolferth and Wood&nbsp;first&nbsp;described the usages of additional chest leads for the diagnosis of myocardial infarction using the leads IV, V, and VI in 1932[1] and by 1938 the standard nomenclature and position of the V-leads was described in a joint paper from the American Heart Association and the Cardiac Society of Great Britain and Ireland[2].<br /><br />Since 1938, there has been little focus in validating the classical precordial lead placement. Instead, efforts to improve the sensitivity and specificity of the 12-Lead ECG focused on adding new electrodes[3,4,5] or improving existing morphological and ST-segmental criteria[6].<br /><br />In 1971, the concept of body surface potential mapping (BSPM) was introduced as an alternative to the standard 12-Lead ECG [7], and by the 1980's it was recognized as providing larger gains in sensitivity in acute myocardial infarction detection over the usage of the classical precordial leads[8]. However, BSPM relies on expensive recording and post-processing techniques, and is cumbersome in its requirement for a large electrode vest which envelops the chest of the patient.<br /><table align="center" cellpadding="0" cellspacing="0" class="tr-caption-container" style="margin-left: auto; margin-right: auto; text-align: center;"><tbody><tr><td style="text-align: center;"><a href="http://2.bp.blogspot.com/-5uo9ZjuXhZg/USVkh7BtfDI/AAAAAAAACUs/qIFFTQY0JJM/s1600/BSPM-Figure.png" imageanchor="1" style="margin-left: auto; margin-right: auto;"><img border="0" height="311" src="http://2.bp.blogspot.com/-5uo9ZjuXhZg/USVkh7BtfDI/AAAAAAAACUs/qIFFTQY0JJM/s400/BSPM-Figure.png" width="400" /></a></td></tr><tr><td class="tr-caption" style="text-align: center;"><b>Figure 1: 80-Lead body surface potential mapping locations.</b></td></tr></tbody></table>In 1985 the first paper on improving the positions of the precordial leads using BSPM was introduced by Drs. Kornreich et al[9]. They explored electrode locations which provided higher degrees of sensitivity and specificity than the traditional precordial lead placement and continued their research into 2008 with a paper describing 4 additional leads which could be added to the traditional 10 electrodes to provide information similar to that of a BSPM[10].<br /><br />Research in 2002 by Drs Kors and Herpen found that moving only two precordial electrodes (V4 and V6) was required to transform the 6 precordial electrodes into a viable interpolated BSPM[11]. Their paper was notable in it sought to find the minimal derangement of the classical positioning in order to obtain diagnostic results.<br /><br />In 2007 and 2008, Drs. Finlay et al explored alternative precordial lead placement using a data driven approach which sought to improve the sensitivity and specificity of MI, LVH, and other ECG abnormalities[12,13]. As with prior research, they proved again that the classical precordial lead positions perform poorly when compared to interpolated BSPMs, however, they acknowledged their improved lead positions were not practical in clinical application. Also of note, Drs. Finlay et al commented that any change to the precordial lead placement would be, "unlikely to succeed because the familiar format of the 12-lead ECG coupled with the considerable amount of diagnostic criteria accumulated in the literature mean that it is a tool with which most clinicians are extremely comfortable and which they are therefore unlikely to relinquish."[14]<br /><br />However, in 2011, Drs. Peter Scott et al demonstrated a simple repositioning of the precordial electrodes which not only improved sensitivity and specificity of acute myocardial infarction identification, but also could be performed in a practical manner[15]. Using data derived from 80-lead BSPM tracings, they performed analysis which found the most appropriate positions of the precordial leads to be located along a horizontal line beginning from V1 and V2 and extending along to the midaxillary.<br /><br /><table align="center" cellpadding="0" cellspacing="0" class="tr-caption-container" style="margin-left: auto; margin-right: auto; text-align: center;"><tbody><tr><td style="text-align: center;"><a href="http://1.bp.blogspot.com/-zyyj37GN9lA/USVkbeKB5jI/AAAAAAAACUk/6Q6W9djgMnM/s1600/BSPM-Optimized.png" imageanchor="1" style="margin-left: auto; margin-right: auto;"><img border="0" height="257" src="http://1.bp.blogspot.com/-zyyj37GN9lA/USVkbeKB5jI/AAAAAAAACUk/6Q6W9djgMnM/s400/BSPM-Optimized.png" width="400" /></a></td></tr><tr><td class="tr-caption" style="text-align: center;"><b>Figure 2: Optimal location of the precordial leads V1-V6 for the detection of acute myocardial infarction.</b></td></tr></tbody></table>This paper has a high potential to challenge the <i>status quo</i> in not only pre-hospital acquisition of 12-Lead electrocardiograms but also in-hospital. The electrode positions given are simple to apply, and could provide for a lesser degree of&nbsp;inter-operator&nbsp;variability in positioning. More importantly, this optimized placement provided for a higher sensitivity and specificity across all types of myocardial infarction.<br /><br />In personal correspondence with Dr. Scott, I inquired as to the changes this presented to other common uses of the 12-Lead ECG--such as bundle branch block definitions or VT vs SVT algorithms--and he related that this research served to open the door to further research into the practical clinical benefits.<br /><ul><li><b>Does the evidence support challenging traditional precordial lead placement?</b></li><li><b>What possible limitations does this lead placement present?</b></li><li><b>What barriers exist to the adoption of this lead placement today?</b></li></ul><b><span style="font-size: x-small;">References</span></b><br /><ol><li><span style="font-size: x-small;">Wolferth CC, Wood FC. The electrocardiographic diagnosis of coronary occlusion by the use of chest leads. Am J Med Sci 1932;183:30-35.</span></li><li><span style="font-size: x-small;">Barnes AR, Pardee HEB, White PD, et al. Standardization of precordial leads. Am Heart J 1938;15:235-239.</span></li><li><span style="font-size: x-small;">Perloff JK. The Recognition of Strictly Posterior Myocardial Infarction by Conventional Scalar Electrocardiography. Circ 1964;30:706-718. [<a href="http://circ.ahajournals.org/content/30/5/706.abstract">FullText</a>]</span></li><li><span style="font-size: x-small;">Erhardt LR, Sjogrn A, Wahlberg I. Single right-sided precordial lead in the diagnosis of right ventricular involvement in inferior myocardial infarction. Am Heart J 1976;91:571-6. [<a href="http://www.ncbi.nlm.nih.gov/pubmed/1266713">PubMed</a>]</span></li><li><span style="font-size: x-small;">Zalenski RJ, Cook D, Rydman R. Assessing the diagnostic value of an ECG containing leads V4R, V8, and V9: The 15-lead ECG. Ann Emerg Med 1993;22:786-793. [<a href="http://www.ncbi.nlm.nih.gov/pubmed/8470834">PubMed</a>]</span></li><li><span style="font-size: x-small;">O'Gara PT, Kushner FG, Ascheim DD, et al. 2013 ACCF/AHA Guideline for the Management of ST-Elevation Myocardial Infarction: A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circ 2013;127:e362-e425. [<a href="http://circ.ahajournals.org/content/127/4/e362.full">FullText</a>]</span></li><li><span style="font-size: x-small;">Barr RC. Selection of the Number and Positions of Measuring Locations for Electrocardiography. IEEE Trans Biomed Eng 1971;18(2):125-138.</span></li><li><span style="font-size: x-small;">Kornreich F, Rautaharju PM. The missing waveform and diagnostic information in the standard 12 lead electrocardiogram. J Electrocardiol 1981;14(4):341-50. [<a href="http://www.ncbi.nlm.nih.gov/pubmed/7299304">PubMed</a>]</span></li><li><span style="font-size: x-small;">Kornreich F, Rautaharju PM, Warren J, et al.&nbsp;Identification of best electrocardiographic leads for diagnosing myocardial infarction by statistical analysis of body surface potential maps. Am J Cardiol 1985;56(13):852-6. [<a href="http://www.ncbi.nlm.nih.gov/pubmed/4061325">PubMed</a>]</span></li><li><span style="font-size: x-small;">Kornreich F, MacLeod RS, Lux RL. Supplemented standard 12-lead electrocardiogram for optimal diagnosis and reconstruction of significant body surface map patterns. J Electrocordiol 2008;41(3):251-6. [<a href="http://www.ncbi.nlm.nih.gov/pubmed/18433616">PubMed</a>]</span></li><li><span style="font-size: x-small;">Kors JA, van Herpen G. How many electrodes and where? A "poldermodel" for electrocardiography. J Electrocardiol 2002;35 Suppl:7-12. [<a href="http://www.ncbi.nlm.nih.gov/pubmed/12539094">PubMed</a>]</span></li><li><span style="font-size: x-small;">Finlay DD, Nugent CD, Kors JA, et al. Optimizing the 12-lead electrocardiogram: a data driven approarch to locating alternative recording sites. J Electrocardiol 2007;40(3):292-9. [<a href="http://www.ncbi.nlm.nih.gov/pubmed/17292383">PubMed</a>]</span></li><li><span style="font-size: x-small;">Finlay DD, Nugent CD, Donnelly MP, Black ND.&nbsp;Selection of optimal recording sites for limited lead body surface potential mapping in myocardial infarction and left ventricular hypertrophy. J Electrocardiol 2008;41(3):264-71. [<a href="http://www.ncbi.nlm.nih.gov/pubmed/18433618">PubMed</a>]</span></li><li><span style="font-size: x-small;"><i>Ibid</i>. 12.</span></li><li><span style="font-size: x-small;">Scott PJ, Navarro C, Stevenson M, et al.&nbsp;Optimization of the precordial leads of the 12-lead electrocardiogram may improve detection of ST-segment elevation myocardial infarction. J Electrocardiol 2011;44(4):425-431. [<a href="http://www.ncbi.nlm.nih.gov/pubmed/21704220">PubMed</a>]</span></li></ol>Christopherhttp://www.blogger.com/profile/11415988855392944633noreply@blogger.com0tag:blogger.com,1999:blog-8723582074539021948.post-1952782520357648472012-07-27T09:22:00.000-04:002012-07-27T09:22:07.171-04:00Synchronized Cardioversion: What Happened?EMS was dispatched for a 62 year old male with an altered mental status. Upon their arrival they found the patient to be non-communicative, responsive to verbal stimuli, in moderate respiratory distress, with pale, diaphoretic skin, and weakly palpable radial pulses. The patient was placed on the monitor during their initial assessment:<br /><br /><table align="center" cellpadding="0" cellspacing="0" class="tr-caption-container" style="margin-left: auto; margin-right: auto; text-align: center;"><tbody><tr><td style="text-align: center;"><a href="http://2.bp.blogspot.com/-HcrJVpS1vJE/UBGsPx00grI/AAAAAAAAB6c/HKiy-jDJwdM/s1600/62yom-VT-rhythm.jpg" imageanchor="1" style="margin-left: auto; margin-right: auto;"><img border="0" height="157" src="http://2.bp.blogspot.com/-HcrJVpS1vJE/UBGsPx00grI/AAAAAAAAB6c/HKiy-jDJwdM/s400/62yom-VT-rhythm.jpg" width="400" /></a></td></tr><tr><td class="tr-caption" style="text-align: center;">Wide complex tachycardia of unknown etiology.</td></tr></tbody></table>A blood pressure was unobtainable, however a pulse of 150 was palpable at the carotid. Labored respirations were present, with clear breath sounds bilaterally.&nbsp;The patient had an extensive cardiac history, renal failure, and insulin dependent diabetes mellitus.&nbsp;The patient's blood sugar was 300 mg/dL.<br /><br />A 12-Lead was obtained and interpreted as presumed ventricular tachycardia:<br /><div><br /></div><table align="center" cellpadding="0" cellspacing="0" class="tr-caption-container" style="margin-left: auto; margin-right: auto; text-align: center;"><tbody><tr><td style="text-align: center;"><a href="http://2.bp.blogspot.com/-Ntuc3oHPUN8/UBGst6Qb_uI/AAAAAAAAB6k/NYMI1I5O8QQ/s1600/62yom-VT-12lead.jpg" imageanchor="1" style="margin-left: auto; margin-right: auto;"><img border="0" height="158" src="http://2.bp.blogspot.com/-Ntuc3oHPUN8/UBGst6Qb_uI/AAAAAAAAB6k/NYMI1I5O8QQ/s400/62yom-VT-12lead.jpg" width="400" /></a></td></tr><tr><td class="tr-caption" style="text-align: center;">Wide complex tachycardia, interpreted as presumed ventricular tachycardia.</td></tr></tbody></table>Differentials of a wide complex tachycardia at 150 bpm include: ventricular tachycardia, SVT with aberrancy, sinus tachycardia with aberrancy, and 2:1 atrial flutter with aberrancy. No previous 12-Lead was available for comparison.<br /><br />Given the presence of a WCT with hemodynamic instability the patient was prepped for synchronized cardioversion. Combo-pads were placed anterio-laterally, the Sync button was pressed, and sync markers were noted with each QRS complex.<br /><br />The patient was then synchronized cardioverted at 100J biphasic:<br /><br /><table align="center" cellpadding="0" cellspacing="0" class="tr-caption-container" style="margin-left: auto; margin-right: auto; text-align: center;"><tbody><tr><td style="text-align: center;"><a href="http://4.bp.blogspot.com/-qNn3kPersO4/UBGuVLhkEMI/AAAAAAAAB6s/q7N4-o35y2s/s1600/62yom-VT-cardioversion-0.jpg" imageanchor="1" style="margin-left: auto; margin-right: auto;"><img border="0" height="150" src="http://4.bp.blogspot.com/-qNn3kPersO4/UBGuVLhkEMI/AAAAAAAAB6s/q7N4-o35y2s/s400/62yom-VT-cardioversion-0.jpg" width="400" /></a></td></tr><tr><td class="tr-caption" style="text-align: center;">100J synchronized cardioversion.</td></tr></tbody></table>A rhythm change was noted on the monitor:<br /><br /><table align="center" cellpadding="0" cellspacing="0" class="tr-caption-container" style="margin-left: auto; margin-right: auto; text-align: center;"><tbody><tr><td style="text-align: center;"><a href="http://1.bp.blogspot.com/-p6SQ6NdvGFI/UBGvd8_EVnI/AAAAAAAAB60/MOu7pFUNXhM/s1600/62yom-VT-cardioversion-1.jpg" imageanchor="1" style="margin-left: auto; margin-right: auto;"><img border="0" height="147" src="http://1.bp.blogspot.com/-p6SQ6NdvGFI/UBGvd8_EVnI/AAAAAAAAB60/MOu7pFUNXhM/s400/62yom-VT-cardioversion-1.jpg" width="400" /></a></td></tr><tr><td class="tr-caption" style="text-align: center;">Ventricular fibrillation post cardioversion.</td></tr></tbody></table>With ventricular fibrillation present, the paramedic disabled synchronization and delivered a 200J biphasic shock:<br /><br /><table align="center" cellpadding="0" cellspacing="0" class="tr-caption-container" style="margin-left: auto; margin-right: auto; text-align: center;"><tbody><tr><td style="text-align: center;"><a href="http://4.bp.blogspot.com/-Tqr1xVHZItA/UBGvfawse4I/AAAAAAAAB68/2Bt7D_ZVZTE/s1600/62yom-VT-defibrillation.jpg" imageanchor="1" style="margin-left: auto; margin-right: auto;"><img border="0" height="152" src="http://4.bp.blogspot.com/-Tqr1xVHZItA/UBGvfawse4I/AAAAAAAAB68/2Bt7D_ZVZTE/s400/62yom-VT-defibrillation.jpg" width="400" /></a></td></tr><tr><td class="tr-caption" style="text-align: center;">200J defibrillation of ventricular fibrillation.</td></tr></tbody></table>After defibrillation, the patient regained consciousness and palpable radial pulses were present. Emergency transport was initiated. During transport, a sustained run of ventricular tachycardia occurred and the patient was given 100 mg lidocaine IV with a subsequent conversion of a sinus rhythm (not captured). The patient experienced multiple episodes of non-sustained ventricular ectopy during transport.<br /><br />In this case the paramedic did not appreciate that oversensing was present from the cardiac monitor's display. It was not until after the summary printed that the ineffective synchronization was discovered.<br /><br /><table align="center" cellpadding="0" cellspacing="0" class="tr-caption-container" style="margin-left: auto; margin-right: auto; text-align: center;"><tbody><tr><td style="text-align: center;"><a href="http://2.bp.blogspot.com/-U3IJaKnSrd0/UBGxR8eL3MI/AAAAAAAAB7E/V_X1BV5LaiY/s1600/62yom-VT-oversensing.jpg" imageanchor="1" style="margin-left: auto; margin-right: auto;"><img border="0" height="168" src="http://2.bp.blogspot.com/-U3IJaKnSrd0/UBGxR8eL3MI/AAAAAAAAB7E/V_X1BV5LaiY/s400/62yom-VT-oversensing.jpg" width="400" /></a></td></tr><tr><td class="tr-caption" style="text-align: center;">Oversensing during synchronized cardioversion--highlighted in red--resulting in therapy delivery during the vulnerable period.</td></tr></tbody></table>As the ventricular myocardium repolarizes, it may not do so homogeonously. This window of non-uniformity, with both absolutely and relatively refractory myocardium present is known as the Vulnerable Period. Electrical stimulation during the vulnerable period of ventricular repolarization may result in ventricular tachyarrhythmias.<br /><br /><table align="center" cellpadding="0" cellspacing="0" class="tr-caption-container" style="margin-left: auto; margin-right: auto; text-align: center;"><tbody><tr><td style="text-align: center;"><a href="http://3.bp.blogspot.com/-RZUNp2vWAk0/UBG9n9YfZYI/AAAAAAAAB7c/4j9hmRwJwMQ/s1600/reilly-fig5.19-vulnerable-period.jpg" imageanchor="1" style="margin-left: auto; margin-right: auto;"><img border="0" height="335" src="http://3.bp.blogspot.com/-RZUNp2vWAk0/UBG9n9YfZYI/AAAAAAAAB7c/4j9hmRwJwMQ/s400/reilly-fig5.19-vulnerable-period.jpg" width="400" /></a></td></tr><tr><td class="tr-caption" style="text-align: center;">Illustration of the vulnerable period of ventricular repolarization. Adapted from Reilly et al. 1998 pp 188 Fig 5.19.</td></tr></tbody></table>This is best appreciated during episodes of a prolonged QT interval. An early-cycle premature ventricular contraction may result in the so called "R-on-T" phenomenon initiating Torsades de Pointes. <br /><br /><table align="center" cellpadding="0" cellspacing="0" class="tr-caption-container" style="margin-left: auto; margin-right: auto; text-align: center;"><tbody><tr><td style="text-align: center;"><a href="https://www.kg-ekgpress.com/ecg_web_brain_DEMO_-_chapter_7_-_qt_interval/" imageanchor="1" style="margin-left: auto; margin-right: auto;" target="_blank"><img border="0" height="118" src="http://3.bp.blogspot.com/-WTQOYUmvOMo/UBHC-yT4mQI/AAAAAAAAB7o/E8ed-lqXUvg/s400/Page_29C-_top-_Torsades_-_ecg.jpg" width="400" /></a></td></tr><tr><td class="tr-caption" style="text-align: center;">A prolonged QT interval and an "R-on-T" PVC resulting in Torsades de Pointes. Used with permission from Dr. Ken Grauer's ECG Web Brain.</td></tr></tbody></table>In this case, the electrical stimulation was provided by inappropriately synchronized biphasic shock. By default the synchronization used Lead II, which featured proportionately smaller negative complexes when compared to their T-waves. Sometimes atrial tachyarrhythmias, such as atrial flutter or atrial fibrillation, may produce deflections sufficient to trigger R-wave deflection as well.<br /><br /><table align="center" cellpadding="0" cellspacing="0" class="tr-caption-container" style="margin-left: auto; margin-right: auto; text-align: center;"><tbody><tr><td style="text-align: center;"><a href="http://4.bp.blogspot.com/-jWTJW2GkPPo/UBG19solwHI/AAAAAAAAB7Q/1BIYlG0zr4c/s1600/65yom-AF-cardioversion-oversensing.jpg" imageanchor="1" style="margin-left: auto; margin-right: auto;"><img border="0" height="206" src="http://4.bp.blogspot.com/-jWTJW2GkPPo/UBG19solwHI/AAAAAAAAB7Q/1BIYlG0zr4c/s400/65yom-AF-cardioversion-oversensing.jpg" width="400" /></a></td></tr><tr><td class="tr-caption" style="text-align: center;">Oversensing of atrial fibrillation. Adapted from Resuscitation 82 (2011):135-136,Fig.1.</td></tr></tbody></table>Appropriate lead section is important when performing synchronized cardioversion in order to avoid delivering the therapy while the myocardium is vulnerable. If synchronization is not accurate the operator of the cardiac monitor should switch leads, increase the gain, or change pad placement.<br /><br /><br /><ul><li><span style="font-size: x-small;">Reilly J. Patrick. Applied Bioelectricity: From Electrical Stimulation to Electropathology. Springer-Verlag: New York (1998); pp 188.</span></li><li><span style="font-size: x-small;">Dr. Ken Grauer's ECG Web Brain. Accessed online 26 July 2012. [<a href="https://www.kg-ekgpress.com/">https://www.kg-ekgpress.com/</a>]</span></li><li><span style="font-size: x-small;">Sodeck GH, Huber J, Stollberger C. Letter to the Editor: Electrical cardioversion - Misinterpretation of the R-wave. Resuscitation 82 (2011): 135-136. [<a href="http://www.ncbi.nlm.nih.gov/pubmed/21036451" target="_blank">PubMed</a>]</span></li></ul>Christopherhttp://www.blogger.com/profile/11415988855392944633noreply@blogger.com12tag:blogger.com,1999:blog-8723582074539021948.post-51501822277434103102012-07-18T15:44:00.001-04:002012-07-18T15:46:08.429-04:00Incidence of cardiac rhythms as determined by Paramedics on an ALS ambulance<p>The following are the incidence of various cardiac rhythms as determined by the treating Paramedic for an ALS ambulance from October 2007 to June 2012. Outlier data were examined for correctness, including all interpretations of rhythms with less than 2% incidence. Incomplete data for each record was added if available, otherwise the record was ignored. AV Nodal Blocks and Bundle Branch Blocks were not recorded in this data set.</p><ul><li>Patients: 3528 (47% male)</li></ul><ul><li>Age: 8 hours - 110 years (avg 56 yr, median 60 yr)</li></ul><br /><div class="separator" style="clear: both; text-align: center;"><a href="http://2.bp.blogspot.com/-JTqZf4Uv5Lw/UAcP9BcXmJI/AAAAAAAAB6I/VSLY3XlpgKc/s1600/leland-ecg-histogram-age-gender.png" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="237" src="http://2.bp.blogspot.com/-JTqZf4Uv5Lw/UAcP9BcXmJI/AAAAAAAAB6I/VSLY3XlpgKc/s400/leland-ecg-histogram-age-gender.png" width="400" /></a></div><div class="separator" style="clear: both; text-align: left;"></div><ul><li>First Contact Heart Rate (&gt;0): 22-260 bpm (avg 91 bpm, median 90 bpm, stdev 29.5)</li></ul><br /><div class="separator" style="clear: both; text-align: center;"><a href="http://3.bp.blogspot.com/-kcZ60h04iKs/UAcQdAk1n9I/AAAAAAAAB6Q/NUwNnGhkrbs/s1600/leland-ecg-histogram-hr-gender.png" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="255" src="http://3.bp.blogspot.com/-kcZ60h04iKs/UAcQdAk1n9I/AAAAAAAAB6Q/NUwNnGhkrbs/s400/leland-ecg-histogram-hr-gender.png" width="400" /></a></div><br /><ul><li>First Contact Rhythm:</li></ul><div style="clear: both; text-align: center;"><table border="0" align="center"><thead><tr><th>Count</th><th>&nbsp;</th><th>Rhythm</th></tr></thead><tbody><tr><td>1841</td><td>52.18%</td><td>Normal Sinus Rhythm</td></tr><tr><td>995</td><td>28.20%</td><td>Sinus Tachycardia</td></tr><tr><td>145</td><td>4.11%</td><td>Paced Rhythm</td></tr><tr><td>139</td><td>3.94%</td><td>Sinus Bradycardia</td></tr><tr><td>114</td><td>3.23%</td><td>Atrial Fibrillation</td></tr><tr><td>88</td><td>2.49%</td><td>Asystole</td></tr><tr><td>68</td><td>1.93%</td><td>Sinus Arrhythmia</td></tr><tr><td>67</td><td>1.90%</td><td>Atrial Fibrillation w/ RVR</td></tr><tr><td>19</td><td>0.54%</td><td>Pulseless Electrical Activity</td></tr><tr><td>18</td><td>0.51%</td><td>Supraventricular Tachycardia</td></tr><tr><td>11</td><td>0.31%</td><td>Ventricular Fibrillation</td></tr><tr><td>10</td><td>0.28%</td><td>Atrial Flutter</td></tr><tr><td>5</td><td>0.14%</td><td>Ventricular Tachycardia</td></tr><tr><td>4</td><td>0.11%</td><td>Junctional Rhythm</td></tr><tr><td>2</td><td>0.06%</td><td>Idioventricular Rhythm</td></tr><tr><td>1</td><td>0.03%</td><td>Ectopic Atrial Tachycardia</td></tr><tr><td>1</td><td>0.03%</td><td>Junctional Tachycardia</td></tr></tbody></table></div><br />Christopherhttp://www.blogger.com/profile/11415988855392944633noreply@blogger.com2tag:blogger.com,1999:blog-8723582074539021948.post-39271884310598539832012-07-12T21:38:00.000-04:002012-07-12T22:20:22.782-04:00EKG Myth - "Can't be Ventricular Tachycardia with that Axis"<br /><i><a href="http://sixlettervariable.blogspot.com/search/label/EKG%20Myth" target="_blank">This is part of a series of posts detailing common electrocardiogram myths.</a></i><br /><br /><br /><span class="Apple-style-span" style="font-size: large;"><b>Myth</b>: Ventricular Tachycardia always has an extreme axis</span><br /><p>When evaluating a wide complex tachycardia, many providers will look at the QRS axis to rule out ventricular tachycardia if an extreme axis is not present. An extreme right axis deviation, also known as No Man's Land, is easiest to appreciate when leads I, II, and III are almost wholly negative.</p><p><i>The absence of an extreme right axis deviation does not rule out ventricular tachycardia.</i></p><p>In fact, the sensitivity of an extreme right axis deviation may only reach 20%<sup>[1]</sup>. More commonly, VT features a left axis deviation<sup>[2]</sup>.</p><table align="center" cellpadding="0" cellspacing="0" class="tr-caption-container" style="margin-left: auto; margin-right: auto; text-align: center;"><tbody><tr><td style="text-align: center;"><a href="http://2.bp.blogspot.com/-Y8im3CepMRc/T_9s7c-EvLI/AAAAAAAAB5c/lBaz8LPuabo/s1600/VT+Left+Axis+-+Table.png" imageanchor="1" style="margin-left: auto; margin-right: auto;"><img border="0" height="115" src="http://2.bp.blogspot.com/-Y8im3CepMRc/T_9s7c-EvLI/AAAAAAAAB5c/lBaz8LPuabo/s400/VT+Left+Axis+-+Table.png" width="400" /></a></td></tr><tr><td class="tr-caption" style="text-align: center;"><i>In 70% (n=172) of VT cases studied by Brugada et al had a Left axis deviation<sup>[2]</sup>.</i></td></tr></tbody></table><p>As with any cardiac rhythm, the axis is dependent on the origin and subsequent activation of the myocardium.</p><table align="center" cellpadding="0" cellspacing="0" class="tr-caption-container" style="margin-left: auto; margin-right: auto; text-align: center;"><tbody><tr><td style="text-align: center;"><a href="http://2.bp.blogspot.com/-tPRnYG878Lo/T_9w9KISsJI/AAAAAAAAB50/D04AUzDxVQE/s1600/Screen+Shot+2012-07-12+at+8.50.14+PM.png" imageanchor="1" style="margin-left: auto; margin-right: auto;"><img border="0" height="400" src="http://2.bp.blogspot.com/-tPRnYG878Lo/T_9w9KISsJI/AAAAAAAAB50/D04AUzDxVQE/s400/Screen+Shot+2012-07-12+at+8.50.14+PM.png" width="262" /></a></td></tr><tr><td class="tr-caption" style="text-align: center;"><i><span style="font-size: x-small;">VT origin and QRS axis. An apical origin results in a superiorly directed axis in the frontal plane. In contrast, a basal origin leads to an inferior QRS axis (lower panel)<sup>[3]</sup>.</span></i></td></tr></tbody></table><p>In VT arising from the left ventricle, a RBBB-like morphology is most common<sup>[4]</sup>. If the origin is in the apex of the left ventricle near the inferiolateral wall, the classic extreme right axis deviation (right superior axis) will be present. Whereas, if the origin is in the left free wall a right inferior axis deviation will be present<sup>[5]</sup>.</p><table align="center" cellpadding="0" cellspacing="0" class="tr-caption-container" style="margin-left: auto; margin-right: auto; text-align: center;"><tbody><tr><td style="text-align: center;"><a href="http://2.bp.blogspot.com/-xk3HVRbkV8Y/T_9vFl9mxQI/AAAAAAAAB5k/4cRLVw2RgdU/s1600/VT+Right+Axis+and+Inferior+Axis.png" imageanchor="1" style="margin-left: auto; margin-right: auto;"><img border="0" height="400" src="http://2.bp.blogspot.com/-xk3HVRbkV8Y/T_9vFl9mxQI/AAAAAAAAB5k/4cRLVw2RgdU/s400/VT+Right+Axis+and+Inferior+Axis.png" width="271" /></a></td></tr><tr><td class="tr-caption" style="text-align: center;"><i>Two cases of Ventricular Tachycardia with an (A) inferior axis and a (B) right axis deviation<sup>[6]</sup>.</i></td></tr></tbody></table><p>In VT arising from the right ventricle, a LBBB-like morphology is most common<sup>[7]</sup>. If the origin is closer to the septum, a right axis deviation will be present. If the origin is the Right Ventricular Outflow Tract (RVOT), an inferior axis will be present with characteristic broad, monomorphic R-waves in leads II, III, and aVF. RVOT-VT is a common ventricular tachycardia in patients without known cardiac disease<sup>[8]</sup>. In some cases, VT arising from the right ventricle will have a normal axis.</p><table align="center" cellpadding="0" cellspacing="0" class="tr-caption-container" style="margin-left: auto; margin-right: auto; text-align: center;"><tbody><tr><td style="text-align: center;"><a href="http://2.bp.blogspot.com/-MW_5aoRbdQk/T_9vqStKFjI/AAAAAAAAB5s/5KDqD31f-vM/s1600/VT+Normal+Axis.png" imageanchor="1" style="margin-left: auto; margin-right: auto;"><img border="0" height="242" src="http://2.bp.blogspot.com/-MW_5aoRbdQk/T_9vqStKFjI/AAAAAAAAB5s/5KDqD31f-vM/s400/VT+Normal+Axis.png" width="400" /></a></td></tr><tr><td class="tr-caption" style="text-align: center;"><i>VT with a normal axis, misclassified as SVT<sup>[9]</sup>.</i></td></tr></tbody></table><p>Any approach to the diagnosis of a wide complex tachycardia should include ruling in Ventricular Tachycardia if an extreme right axis deviation is present. However, clinicians should be mindful that the absence of an extreme right axis deviation cannot rule out Ventricular Tachycardia.</p><ol><li>Vereckei A, et al. New algorithm using only lead aVR for differential diagnosis of wide QRS complex tachycardia. Heart Rhythm 2008;5:89–98. [<a href="http://www.ncbi.nlm.nih.gov/pubmed/18180024" target="_blank">PubMed</a>]</li><li>Brugada P, et al. A New Approach to the Differential Diagnosis of a Regular Tachycardia with a Wide QRS Complex. Circulation 1991;83:1649-1659. [<a href="http://circ.ahajournals.org/content/83/5/1649.abstract" target="_blank">Full Text PDF</a>]</li><li>Wellens HJJ. Ventricular tachycardia: diagnosis of broad QRS complex tachycardia. Heart 2001;86:579-585. [<a href="http://heart.bmj.com/content/86/5/579.full" target="_blank">Full Text</a>]</li><li>Surawicz B, Knilans TK. Chou's Electrocardiography in Clinical Practice: Adult and Pediatric, 6th ed. Philadelphia, PA. Saunders, 2008.</li><li>Pellegrini CN, Scheinman MM. Clinical Management of Ventricular Tachycardia. Curr Probl Cardiol. 2010;35:453-504. [<a href="http://www.ncbi.nlm.nih.gov/pubmed/20887902" target="_blank">PubMed</a>]</li><li><i>Ibid 2.</i></li><li><i>Ibid 4.</i></li><li><i>Ibid 5.</i></li><li><i>Ibid 2.</i></li></ol>Christopherhttp://www.blogger.com/profile/11415988855392944633noreply@blogger.com8tag:blogger.com,1999:blog-8723582074539021948.post-31453031533628727212012-02-07T17:23:00.000-05:002012-02-08T17:15:04.778-05:00J-waves after ROSC and Intra-arrest Therapeutic HypothermiaThe following is the post-resuscitation 12-Lead electrocardiogram of an 82 year old female who received intra-arrest therapeutic hypothermia, via chilled saline and ice packs, as part of a new protocol for cardiac arrest management. The patient also received three defibrillations and was administered epinephrine, naloxone, and amiodarone during the&nbsp;resuscitation.<br /><br /><table align="center" cellpadding="0" cellspacing="0" class="tr-caption-container" style="margin-left: auto; margin-right: auto; text-align: center;"><tbody><tr><td style="text-align: center;"><a href="http://2.bp.blogspot.com/-WGFRl-688Kw/TzGZWbIndJI/AAAAAAAABzU/iKSaHd-fqZI/s1600/82yo+F+-+Cardiac+Arrest+-+ROSC+-+Initial+12-Lead.jpg" imageanchor="1" style="margin-left: auto; margin-right: auto;"><img border="0" height="151" src="http://2.bp.blogspot.com/-WGFRl-688Kw/TzGZWbIndJI/AAAAAAAABzU/iKSaHd-fqZI/s400/82yo+F+-+Cardiac+Arrest+-+ROSC+-+Initial+12-Lead.jpg" width="400" /></a></td></tr><tr><td class="tr-caption" style="text-align: center;">12-Lead ECG obtained approximately 5 minutes after ROSC</td></tr></tbody></table>The post arrest 12-Lead ECG shows a sinus rhythm with frequent premature atrial and ventricular ectopic complexes. The LifePak 12, which uses the GE Marquette 12SL algorithm, displayed the ominous&nbsp;<b><span style="font-family: 'Courier New', Courier, monospace;">*** ACUTE MI SUSPECTED ***</span></b> message and suggested a lateral injury pattern.<br /><br />Closer inspection of&nbsp;the lateral precordial leads&nbsp;reveals the ST-elevations present are actually giant J-waves, or Osborn waves.<br /><br /><table align="center" cellpadding="0" cellspacing="0" class="tr-caption-container" style="margin-left: auto; margin-right: auto; text-align: center;"><tbody><tr><td style="text-align: center;"><a href="http://4.bp.blogspot.com/-d-NZeDWiSig/TzGbcaCzzLI/AAAAAAAABzc/gtYrbO1ck7o/s1600/82yo+F+-+Cardiac+Arrest+-+V5-V6+Osborn+Waves.jpg" imageanchor="1" style="margin-left: auto; margin-right: auto;"><img border="0" height="162" src="http://4.bp.blogspot.com/-d-NZeDWiSig/TzGbcaCzzLI/AAAAAAAABzc/gtYrbO1ck7o/s320/82yo+F+-+Cardiac+Arrest+-+V5-V6+Osborn+Waves.jpg" width="320" /></a></td></tr><tr><td class="tr-caption" style="text-align: center;">J-waves--or Osborn waves--appreciated in the lateral precordial leads</td></tr></tbody></table>Recognizing this finding is present, a closer look at the entire 12-Lead ECG shows that subtle J-waves are present in almost every lead group.<br /><br /><table align="center" cellpadding="0" cellspacing="0" class="tr-caption-container" style="margin-left: auto; margin-right: auto; text-align: center;"><tbody><tr><td style="text-align: center;"><a href="http://3.bp.blogspot.com/-bvx5Y3wZdsE/TzGdKPltrSI/AAAAAAAABzk/uRx8_YPPwHo/s1600/82yo+F+-+Cardiac+Arrest+-+ROSC+-+Subsequent+12-Lead.jpg" imageanchor="1" style="margin-left: auto; margin-right: auto;"><img border="0" height="161" src="http://3.bp.blogspot.com/-bvx5Y3wZdsE/TzGdKPltrSI/AAAAAAAABzk/uRx8_YPPwHo/s400/82yo+F+-+Cardiac+Arrest+-+ROSC+-+Subsequent+12-Lead.jpg" width="400" /></a></td></tr><tr><td class="tr-caption" style="text-align: center;">Subsequent 12-Lead ECG obtained 17 minutes after ROSC</td></tr></tbody></table>A repeat 12-Lead ECG acquired 12 minutes later shows a sinus tachycardia with a single PAC, without the giant J-waves from the initial ECG, diffuse ST/T-wave changes consistent with ischemia are also present. However, small J-point elevation persists in the lateral precordials. The computerized interpretation no longer believes a STEMI-pattern is present and incorrectly identifies the rhythm as atrial fibrillation. <br /><br /><table align="center" cellpadding="0" cellspacing="0" class="tr-caption-container" style="margin-left: auto; margin-right: auto; text-align: center;"><tbody><tr><td style="text-align: center;"><a href="http://3.bp.blogspot.com/-VXh1x8pbpEw/TzGepgdNYcI/AAAAAAAABzs/x3Fa0Yw2uUA/s1600/82yo+F+-+Cardiac+Arrest+-+Precordial+Comparison.jpg" imageanchor="1" style="margin-left: auto; margin-right: auto;"><img border="0" height="262" src="http://3.bp.blogspot.com/-VXh1x8pbpEw/TzGepgdNYcI/AAAAAAAABzs/x3Fa0Yw2uUA/s400/82yo+F+-+Cardiac+Arrest+-+Precordial+Comparison.jpg" width="400" /></a></td></tr><tr><td class="tr-caption" style="text-align: center;">Comparison of the precordial leads between the first and subsequent 12-Lead ECG.</td></tr></tbody></table>A side by side look at the precordial leads provides an interesting look at the near resolution of the giant J-waves post-ROSC.<br /><br />One explanation for the normalization of the traditional electrocardiographic findings of hypothermia may be related to the management of the patient's&nbsp;ventilation&nbsp;both intra-arrest and post-arrest. As the patient's pH normalized with mechanical ventilation and a perfusing rhythm, so did the repolarization abnormalities (visualized as J-waves).<br /><br /><b><span style="font-size: x-small;">References</span></b><br /><ol><li><span style="font-size: x-small;">Antzelevitch C, Yan GX. J Wave Syndromes. <i>Heart Rhythm</i>. 2010; 7(4):549-558. [<a href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2843811/">FullText</a>]</span></li><li><span style="font-size: x-small;">Fenstad ER, et al. Therapeutic hypothermia in out of hospital sudden cardiac arrest: Significance of J-waves. <i>J Am Coll Cardio</i>. 2011; 57(14):Suppl 5, E1002. [<a href="http://content.onlinejacc.org/cgi/reprint/55/20/2287.pdf">PDF FullText</a>]</span></li><li><span style="font-size: x-small;">Edelman ER, Joynt K. J Waves of Osborn Revisited. <i>J Am Coll Cardio</i>. 2010; 55(20):2287. [<a href="http://www.ncbi.nlm.nih.gov/pubmed/20466208">PubMed</a>]</span></li><li><span style="font-size: x-small;"><a href="http://hqmeded-ecg.blogspot.com/2011/11/osborn-waves-and-hypothermia.html">Dr. Smith's ECG Blog: Osborn Waves and Hypothermia.</a></span></li></ol>Christopherhttp://www.blogger.com/profile/11415988855392944633noreply@blogger.com4tag:blogger.com,1999:blog-8723582074539021948.post-38146762839508112272011-12-26T20:52:00.000-05:002014-08-21T10:01:11.233-04:00Philips Healthcare's Sierra ECG format XLI Compression SchemeOne of the services I work for has recently acquired a <a href="http://www.healthcare.philips.com/us_en/products/resuscitation/products/MRx/mrx_ems.wpd" target="_blank">Philips HeartStart MRx cardiac monitor</a>. It came complete with Bluetooth transmission of 12-Lead and event data. At roughly the same time our service installed a computer, an MDT, into the cab of our unit to interface with our county's <a href="http://en.wikipedia.org/wiki/Computer-aided_dispatch" target="_blank">CAD software</a>.<br /><br />Naturally I linked our monitor and our MDT via Bluetooth, and transmitted a 12-Lead from a rhythm generator. When the file landed on the MDT, I looked for an application to view the 12-Leads and rhythm strips, however, none appeared to be able to use the file as-is.<br /><br />For the non-technical, the ECGs are shipped compressed--somewhat like a ZIP file--which contains all of your monitored vital signs, printed rhythm strips, and your 12-Leads. The format of the 12-Leads is an Open Standard; Philips Healthcare provides most of the details needed to use the files. The 12-Lead data is also compressed to save space. Unfortunately, there is no documentation which tells you how to decompress the 12-Lead data.<br /><br /><i>The technically-faint-of-heart should <a href="https://www.blogger.com/blogger.g?blogID=8723582074539021948#end">skip these next bits</a>.</i><br /><br />For the technical, the ECGs are contained in a Gzip'd TAR archive. The 12-Leads are stored inside in an XML format known as the Sierra ECG format (currently at version 1.03 or 1.04, as far as I can tell). Inside this XML format is Base64 encoded, XLI compressed data comprising the acquired leads during a 12-Lead (up to 16 leads appear to be able to be stored).<br /><br />I searched for a description of the XLI compression format, however, I was only able to find a reference implementation for Microsoft Windows which simply decoded the files. No code or description was provided, and the implementation itself is not portable. <i>(ed: it appears this may be a reference to the HP PageWriter XLi which Philips acquired)</i><br /><br />At this point I decided my only option was to reverse engineer the XLI Compression format, and began with simple guesses. I tried decompressing the data using Deflate, Zip, and RLE without any progress. I was able to determine that the first 8 bytes of the compressed data included a compressed length, some uncompressed data, and that each of the 12 to 16 leads were stored in a chunk with one of these headers:<br /><blockquote class="tr_bq"><pre>offset 2 4 6 8 ...<br />+--------+--------+--------+--------+--------+--------+--------+<br />| Size | Unk. | Delta? | Compressed data... |<br />+--------+--------+--------+--------+ |<br />| ... [Size bytes] |<br />+--------+--------+--------+--------+--------+--------+--------+<br />| Next lead chunk ... |</pre></blockquote>Once the simple guesses were ruled out, I began exploring the behavior of the reference implementation provided for the Sierra ECG format. Using&nbsp;<a href="http://www.ollydbg.de/">OllyDbg</a>&nbsp;I noticed certain code tells which made me believe the decompression algorithm read 10-bits at a time:<br /><blockquote class="tr_bq"><pre>SHR EAX, 16h ; reduce EAX to the 10-bit code word<br />SHL ECX, Ah ; prepare to read 10 more bits from the input</pre></blockquote>The compressed data also did not appear to contain a compression dictionary referenced by the code. At this point I considered I was looking at a form of <a href="http://en.wikipedia.org/wiki/Lempel%E2%80%93Ziv%E2%80%93Welch" target="_blank">Lempel-Ziv-Welch</a>, or LZW, compression. LZW is a popular, lossless compression scheme which creates its compression dictionary on the fly. It is used by the <a href="http://en.wikipedia.org/wiki/Graphics_Interchange_Format" target="_blank">GIF</a> and <a href="http://en.wikipedia.org/wiki/Tagged_Image_File_Format#Part_2:_TIFF_Extensions" target="_blank">TIFF</a> image formats, and was the subject of controversy when it was first introduced into the GIF format due to patent licensing requirements.<br /><br />In my quest to quickly reach a conclusion I found an <a href="http://marknelson.us/1989/10/01/lzw-data-compression/" target="_blank">excellent LZW implementation from Mark Nelson in C</a> and it successfully decompressed the data. In fact, the structure of the C code was so familiar, I realized <i>the reference implementation from Philips used the exact same code!</i><br /><br />If you've reached this step while following along at home, you'll notice the decompressed data seems front-loaded with 0's. This is a case of intelligently streaming the data to the compression algorithm to take advantage of data duplication.<br /><br />The uncompressed data represents 16-bit delta codes, of which the majority include 0x00 or 0xFF in their most significant byte (MSB). This is because they are either small and positive or small and negative, and as ECG data is rhythmic the delta codes are likely to retain the same sign for numerous samples.<br /><br />To take advantage of this fact during compression, the delta codes are first deinterleaved into two halves. The first half includes each MSB and the second half includes each LSB. The pseudo-code for interleaving the decompressed data looks like the following:<br /><blockquote class="tr_bq"><pre># input contains the decompressed data<br /># output will contain the interleaved 16-bit delta codes<br />fun unpack( input[], output[], nSamples )<br /> for i &lt;- 1..nSamples<br /> output[i] &lt;- (input[i] &lt;&lt; 8) | input[nSamples + i]<br /> endfor<br />endfun</pre></blockquote>At this point the delta compression scheme will need to be decoded to produce the actual signal data for each of the leads. The delta compression scheme is a simple recurrence relation (a second order difference relation) using the prior two delta codes: <br /><blockquote class="tr_bq"><pre># output contains the 16-bit delta codes<br /># first is the 16-bit delta code from the chunk header<br />fun deltaDecompression( output[], nSamples, first )<br /> x &lt;- output[1]<br /> y &lt;- output[2]<br /> prev &lt;- first<br /> for i &lt;- 3..nSamples<br /> z &lt;- (2 * y) - x - prev<br /> prev &lt;- output[i] - 64 # is -64 to 64 the range?<br /> output[i] &lt;- z<br /> x &lt;- y<br /> y &lt;- z<br /> endfor<br />endfun</pre></blockquote>Now that you have the actual, per signal data all you need to do is recreate leads III, aVR, aVL, and aVF. This is done using the data from leads I and II as on most ECG machines. I've omitted the actual formulas for brevity.<br /><br />Using <a href="https://github.com/sixlettervariables/sierra-ecg-tools/wiki" id="end" name="end">my reference implementation of the decompression algorithm</a> I was able to feed the original acquired 12-Lead to the <a href="http://openmedical.sed.hu/en/szoftverek/konverterek/3" target="_blank">Philips ECG to SVG converter</a>, with the following results: <br /><br /><div class="separator" style="clear: both; text-align: center;"><a href="http://2.bp.blogspot.com/-m-gWufEnaqA/Tvki_7nve8I/AAAAAAAABzM/ONDlVoJNc8w/s1600/jv5wL.png" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" src="http://2.bp.blogspot.com/-m-gWufEnaqA/Tvki_7nve8I/AAAAAAAABzM/ONDlVoJNc8w/s400/jv5wL.png" height="302" width="400" /></a></div><br />If you'd like to start playing with my code I welcome you to join my <a href="https://github.com/sixlettervariables/sierra-ecg-tools">Github Project: sierra-ecg-tools</a>. I am also working on a C implementation, and likely an Android implementation. Stay tuned, and apologies for the technical post.<br /><br /><i>The author has no financial ties to Philips Healthcare and received no compensation for this work.</i>Christopherhttp://www.blogger.com/profile/11415988855392944633noreply@blogger.com2Wilmington, NC, USA34.2257255 -77.944710234.120694500000006 -78.1026387 34.3307565 -77.7867817tag:blogger.com,1999:blog-8723582074539021948.post-78182054150335596742011-12-06T16:20:00.001-05:002011-12-06T18:03:11.711-05:00EKG Myth - Ventricular tachycardia must have concordance<i><a href="http://sixlettervariable.blogspot.com/search/label/EKG%20Myth">This is part of a series of posts detailing common electrocardiogram myths.</a></i><br /><br /><br /><span class="Apple-style-span" style="font-size: large;"><b>Myth</b>: Ventricular Tachycardia&nbsp;must have precordial concordance</span><br /><br />When differentiating a regular, wide-complex tachycardia some will look for precordial concordance to rule-in, or more importantly to rule-out ventricular tachycardia.<br /><br />The absence of precordial concordance is not a reliable method of ruling out ventricular tachycardia:<br /><blockquote class="tr_bq">Although the specificity of concordance for VT is high (&gt;90%), the sensitivity is low (~20%)<sup>1</sup>.</blockquote>It is generally thought that positive concordance indicates a posteriobasal left ventricular origin and negative concordance indicates an anterioapical left ventricular origin.&nbsp;However, in the case of positive concordance, SVT with a left-posterior accessory pathway is a known cause.<br /><br />Until recently, negative concordance has been thought to be "virtually diagnostic" of ventricular tachycardia<sup>2</sup>. Multiple case reports have shown that certain configurations of accessory pathways can also cause negative concordance<sup>3,4,5</sup>.<br /><br />The key takeaway is while this criteria is a useful tool to rule-in ventricular tachycardia (i.e.&nbsp;<i>high&nbsp;specificity</i>), it is not a useful tool to rule-out ventricular tachycardia (i.e.&nbsp;<i>low sensitivity</i>).<br /><br /><table align="center" cellpadding="0" cellspacing="0" class="tr-caption-container" style="margin-left: auto; margin-right: auto; text-align: center;"><tbody><tr><td style="text-align: center;"><a href="http://1.bp.blogspot.com/-bl7dI3jJGSg/Tt6WaxXjGcI/AAAAAAAABy4/ZRJY2q8tRy4/s1600/WCT+-+VT+-+Concordance.png" imageanchor="1" style="margin-left: auto; margin-right: auto;"><img border="0" height="272" src="http://1.bp.blogspot.com/-bl7dI3jJGSg/Tt6WaxXjGcI/AAAAAAAABy4/ZRJY2q8tRy4/s400/WCT+-+VT+-+Concordance.png" width="400" /></a></td></tr><tr><td class="tr-caption" style="text-align: center;">Ventricular tachycardia without precordial concordance<sup>6</sup>.</td></tr></tbody></table><table align="center" cellpadding="0" cellspacing="0" class="tr-caption-container" style="margin-left: auto; margin-right: auto; text-align: center;"><tbody><tr><td style="text-align: center;"><a href="http://ems12lead.com/2011/11/90-year-old-female-cc-seizur/" imageanchor="1" style="margin-left: auto; margin-right: auto;" target="_blank"><img border="0" height="160" src="http://ems12lead.com/files/2011/11/90yo-F-Seizure-Initial-12-Lead1.png" width="400" /></a></td></tr><tr><td class="tr-caption" style="text-align: center;">Ventricular tachycardia without precordial concordance. (c) 2011 EMS 12-Lead Blog.</td></tr></tbody></table><table align="center" cellpadding="0" cellspacing="0" class="tr-caption-container" style="margin-left: auto; margin-right: auto; text-align: center;"><tbody><tr><td style="text-align: center;"><a href="http://1.bp.blogspot.com/-zLSGswyeRXA/Tt6XvI_jExI/AAAAAAAABzA/koj4Lmy7CJw/s1600/WCT+-+AFlutter+-+Concordance.png" imageanchor="1" style="margin-left: auto; margin-right: auto;"><img border="0" height="182" src="http://1.bp.blogspot.com/-zLSGswyeRXA/Tt6XvI_jExI/AAAAAAAABzA/koj4Lmy7CJw/s400/WCT+-+AFlutter+-+Concordance.png" width="400" /></a></td></tr><tr><td class="tr-caption" style="text-align: center;">WPW and Atrial flutter with positive concordance<sup>7</sup>.</td></tr></tbody></table>While positive or negative concordance may strongly suggest ventricular tachycardia, providers should not rule-out ventricular tachycardia in its absence.<br /><br /><ol><li>Pellegrini CN, Scheinman MM. Clinical management of ventricular tachycardia. <i>Curr Probl Cardiol</i>. 2010; 35(9):453-504. [<a href="http://www.ncbi.nlm.nih.gov/pubmed/20887902" target="_blank">PubMed</a>]</li><li>Goldberger ZD, Rho RW, Page RL. Approach to the Diagnosis and Initial Management of the Stable Adult Patient With a Wide Complex Tachycardia. <i>Am J Cardiol</i>. 2008; 101:1456-1466. [<a href="http://www.sciencedirect.com/science/article/pii/S000291490800163X" target="_blank">Full Text</a>]</li><li>Pappas LK, et al. Wide QRS complex supraventricular tachycardia with negative precordial concordance. <i>Am Heart Hosp J</i>. 2009; 7(1):67-8. [<a href="http://www.ncbi.nlm.nih.gov/pubmed/19742439" target="_blank">PubMed</a>]</li><li>Kappos KG, et al. Wide QRS Complex tachycardia with a negative concordance pattern in the precordial leads: Are the ECG criteria always reliable? <i>Pacing Clin Electrophys</i>. 2006; 29:63-6. [<a href="http://www.ncbi.nlm.nih.gov/pubmed/16441720" target="_blank">PubMed</a>]</li><li>Volders PGA, et al. Wide QRS complex tachycardia with negative precordial concordance: Always a ventricular origin? <i>J Cardio Electro.</i>&nbsp;2003; 14:109-111. [<a href="http://www.ncbi.nlm.nih.gov/pubmed/12625622" target="_blank">PubMed</a>]</li><li>Garmel GM. Wide Complex Tachycardias: Understanding this Complex Condition Part 1 - Epidemiology and Electrophysiology. <i>W J Emerg Med</i>. 2008; 9(1):28-39. [<a href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2672229/" target="_blank">Full Text</a>]</li><li>Ibid. 1, Figure 3.</li></ol>Christopherhttp://www.blogger.com/profile/11415988855392944633noreply@blogger.com2tag:blogger.com,1999:blog-8723582074539021948.post-34094317403134291002011-11-17T06:56:00.001-05:002011-12-09T13:08:14.448-05:00EKG Myth - "It's Too Fast for Ventricular Tachycardia"<i><a href="http://sixlettervariable.blogspot.com/search/label/EKG%20Myth">This is part of a series of posts detailing common electrocardiogram myths.</a></i><br /><i><br /></i><br /><span class="Apple-style-span" style="font-size: large;"><b>Myth</b>: Rate can help you rule out Ventricular Tachycardia</span><br /><br />When differentiating a regular, wide-complex tachycardia some will look at the rate to rule out ventricular tachycardia. Studies have not found rate to be a predictive finding<sup>1</sup>.<br /><blockquote class="tr_bq"><blockquote class="tr_bq">...regarding ventricular rate, significant overlap unfortunately exists between VT and SVT such that rate is not a helpful criterion to differentiate origins<sup>2</sup>.</blockquote></blockquote>Ventricular tachycardia technically can range in rates from 100 bpm through 300 bpm.&nbsp;However, a practical definition of VT would place the lower bound around 120 bpm and the upper bound around 260 bpm<sup>3</sup>.<br /><br />Common terminology includes rates slower than 120 as "Slow Ventricular Tachycardia", which most often is not true VT<sup>4</sup>. Rates upwards of 260 to 300 bpm are commonly termed "Ventricular Flutter"<sup>5</sup>.<br /><br /><table align="center" cellpadding="0" cellspacing="0" class="tr-caption-container" style="margin-left: auto; margin-right: auto; text-align: center;"><tbody><tr><td style="text-align: center;"><a href="http://ecg.bidmc.harvard.edu/maven/dispcase.asp?rownum=342&amp;caseid=343" imageanchor="1" style="margin-left: auto; margin-right: auto;" target="_blank"><img border="0" height="202" src="http://ecg.bidmc.harvard.edu/mavendata/images/case343/1350x900.gif" width="400" /></a></td></tr><tr><td class="tr-caption" style="text-align: center;">Ventricular tachycardia at 130 bpm. (c) 2001 - 2011 Beth Israel Deaconess Medical Center.</td></tr></tbody></table><br /><table align="center" cellpadding="0" cellspacing="0" class="tr-caption-container" style="margin-left: auto; margin-right: auto; text-align: center;"><tbody><tr><td style="text-align: center;"><a href="http://ems12lead.com/2011/11/90-year-old-female-cc-seizur/" imageanchor="1" style="margin-left: auto; margin-right: auto;" target="_blank"><img border="0" height="161" src="http://ems12lead.com/files/2011/11/90yo-F-Seizure-Initial-12-Lead1.png" width="400" /></a></td></tr><tr><td class="tr-caption" style="text-align: center;">Ventricular tachycardia at 206 bpm. (c) 2011 EMS 12-Lead Blog.</td></tr></tbody></table><br /><table align="center" cellpadding="0" cellspacing="0" class="tr-caption-container" style="margin-left: auto; margin-right: auto; text-align: center;"><tbody><tr><td style="text-align: center;"><a href="http://emedicine.medscape.com/article/159075-overview" imageanchor="1" style="margin-left: auto; margin-right: auto;" target="_blank"><img border="0" height="182" src="http://img.medscape.com/pi/emed/ckb/cardiology/150072-159075-162.jpg" width="400" /></a></td></tr><tr><td class="tr-caption" style="text-align: center;">Ventricular tachycardia at 280 bpm. (c) 1994-2011 WebMD.</td></tr></tbody></table><br />As a rule: a regular, wide-complex tachycardia should be treated as ventricular tachycardia in the field, until proven otherwise.<br /><br /><ol><li>Griffith MJ, et al. Multivariate analysis to simplify the differential diagnosis of broad complex tachycardia. Br Heart J (1991); 66:166-74. [<a href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1024611/" target="_blank">PubMed</a>]</li><li>Hudson KB, et al. Electrocardiographic Manifestations: Ventricular Tachycardia. J Emerg Med (2003); 25:303-314. [<a href="http://www.ncbi.nlm.nih.gov/pubmed/14585460" target="_blank">PubMed</a>]</li><li>Surawicz B, Knilans TK. Chou's Electrocardiography in Clinical Practice: Adult and Pediatric, 6th ed. Philadelphia, PA. Saunders, 2008.&nbsp;</li><li>Mattu A. ECG PEARLS: Beware the Slow Mimics of Ventricular Tachycardia. Emergency Physicians Monthly, 24 August 2010. Retrieved Online 8 November 2011. [<a href="http://www.epmonthly.com/clinical-skills/ekg/ecg-pearls-beware-the-slow-mimics-of-ventricular-tachycardia/" target="_blank">Free Full Text</a>]</li><li>Gurevitz O, et al. Long-term prognosis of inducible ventricular flutter: not an innocent finding. Am Heart J (2004); 147(4):649-54. [<a href="http://www.ncbi.nlm.nih.gov/pubmed/15077080" target="_blank">PubMed</a>]</li></ol>Christopherhttp://www.blogger.com/profile/11415988855392944633noreply@blogger.com3tag:blogger.com,1999:blog-8723582074539021948.post-23076467656718459212011-06-22T19:31:00.000-04:002011-06-22T19:31:52.034-04:00Zebra SpottingI'm sure we all received the following good advice at some point in our EMS education or careers:<br /><blockquote>"When you hear hoofbeats, think horses not zebras."</blockquote>I propose we add the corollary:<br /><blockquote>"...but if you don't stay to watch, you won't know what you missed."</blockquote><a href="http://www.washingtontimes.com/news/2011/jun/8/dcs-ig-faults-paramedic-response-2008-acid-reflux-/">Remember, always err on the side of the patient.</a>Christopherhttp://www.blogger.com/profile/11415988855392944633noreply@blogger.com0tag:blogger.com,1999:blog-8723582074539021948.post-85033550364349443822011-05-23T09:36:00.001-04:002012-03-08T15:27:01.144-05:00An attempt at Video Education: Axis DeterminationI'm a huge fan of the <a href="http://www.khanacademy.org/" target="_blank">Khan Academy</a> and regularly watch his videos when I have a question about something in mathematics. Usually it only takes five or so minutes into the video for me to recall how to accomplish the task, and I can move along. I've always wanted to see if I could do the same thing for ECG interpretation.<br />So here is my inaugural attempt; rapid axis determination using leads I and aVF (assuming you're ok with a ±5° difference):<br /><object style="height: 390px; width: 640px;"><param name="movie" value="http://www.youtube.com/v/kOdk20FgcC0?version=3" /><param name="allowFullScreen" value="true" /><param name="allowScriptAccess" value="always" /><embed allowfullscreen="true" allowscriptaccess="always" height="390" src="http://www.youtube.com/v/kOdk20FgcC0?version=3" type="application/x-shockwave-flash" width="640"></embed></object>Christopherhttp://www.blogger.com/profile/11415988855392944633noreply@blogger.com6tag:blogger.com,1999:blog-8723582074539021948.post-5108359744572201982011-04-06T11:29:00.001-04:002011-04-06T11:29:13.587-04:00Conclusion to 54 year old female CC: BLS intercept<blockquote><span class="Apple-style-span" style="font-family: inherit;">As many readers noted, there is a lot of baseline wander. This is not the most helpful of 12-Leads. On scene the crew attempted multiple 12-Leads, however, the patient would not sit still and that was the best one.&nbsp;</span></blockquote><blockquote><span class="Apple-style-span" style="font-family: inherit;">I think a close look at the Initial 12-Lead has enough information to make a field diagnosis.</span></blockquote><div style="background-attachment: initial; background-clip: initial; background-color: transparent; background-image: initial; background-origin: initial; border-bottom-width: 0px; border-color: initial; border-left-width: 0px; border-right-width: 0px; border-style: initial; border-top-width: 0px; margin-bottom: 18px; margin-left: 0px; margin-right: 0px; margin-top: 0px; outline-color: initial; outline-style: initial; outline-width: 0px; padding-bottom: 0px; padding-left: 0px; padding-right: 0px; padding-top: 0px; vertical-align: baseline;"><span class="Apple-style-span" style="font-family: inherit;"><a href="http://ems12lead.com/2011/04/06/54-year-old-female-cc-bls-intercept-conclusion/">Read the rest at EMS 12-Lead Blog: 54 year old female CC: BLS intercept - Conclusion</a>!</span></div>Christopherhttp://www.blogger.com/profile/11415988855392944633noreply@blogger.com2tag:blogger.com,1999:blog-8723582074539021948.post-91408320479843413812011-04-05T12:51:00.000-04:002011-04-05T12:51:54.790-04:00New Case Study at EMS 12-Lead BlogMy first case study as an associate editor is up at <a href="http://ems12lead.com/2011/04/04/54-year-old-female-cc-bls-intercept/">the EMS 12-Lead Blog, so check it out: 54 year old female cc: BLS Intercept</a>:<br /><blockquote><div><span class="Apple-style-span" style="color: #eeeeee; line-height: 18px;">"It is just after 3am when you are called to intercept a BLS unit on scene with a 54 year old female with a low heart rate.</span></div><br /><div><span class="Apple-style-span" style="color: #eeeeee; line-height: 18px;">Upon your arrival, you find two EMT-Basics attending to a small woman lying in bed, who appears acutely ill..."</span></div></blockquote>Also, I've done <a href="http://ems12lead.com/2011/04/05/second-degree-or-third-degree/">a brief review of atrioventricular blocks</a> to help with identification of the rhythm in this case study!<br /><br />Enjoy.Christopherhttp://www.blogger.com/profile/11415988855392944633noreply@blogger.com1tag:blogger.com,1999:blog-8723582074539021948.post-74319752737537098042011-03-10T18:54:00.001-05:002011-03-10T19:00:12.814-05:00Unrecognized Limb Lead Misplacement?Dr. Smith's ECG Blog has a new case up, "<a href="http://hqmeded-ecg.blogspot.com/2011/03/reperfusion-through-collaterals.html">Reperfusion through collaterals associated with nitroglycerin, lateral MI with reciprocal T-wave inversion in lead III</a>," with a pretty stark change in the initial 12-Leads. However, I have a hunch the stark change was really a change in the limb lead positions!<br /><br /><table align="center" cellpadding="0" cellspacing="0" class="tr-caption-container" style="margin-left: auto; margin-right: auto; text-align: center;"><tbody><tr><td style="text-align: center;"><a href="https://lh4.googleusercontent.com/-zC0j6QTm_N4/TXlgBNV6mfI/AAAAAAAABvY/4qbRmJrxNuY/s1600/ecg-la-ll-reversal.jpg" imageanchor="1" style="margin-left: auto; margin-right: auto;"><img border="0" height="160" src="https://lh4.googleusercontent.com/-zC0j6QTm_N4/TXlgBNV6mfI/AAAAAAAABvY/4qbRmJrxNuY/s400/ecg-la-ll-reversal.jpg" width="400" /></a></td></tr><tr><td class="tr-caption" style="text-align: center;"><b>ECG 1 and ECG 2: Limb Leads Only</b></td></tr></tbody></table>Look at leads I and II, notice how they "swap" positions between the two 12-Leads. Now look at aVL and aVF, notice how the "swap" positions too. Now take a look at lead III. It goes from inverted P's and T's with a Qr complex, to upright P's and T's with a Rs complex.<br /><br />I propose that this change is due to a simple reversal of two leads.&nbsp;If we take a look at our friend Einthoven's Triangle (<a href="http://sixlettervariable.blogspot.com/2011/02/highlighting-atrial-activity-on-ecg-s5.html">we covered this in a previous post on the S5 Lead</a>) we can see that this makes sense!<br /><br /><table align="center" cellpadding="0" cellspacing="0" class="tr-caption-container" style="margin-left: auto; margin-right: auto; text-align: center;"><tbody><tr><td style="text-align: center;"><a href="https://lh5.googleusercontent.com/-9O6oQ8w9CAU/TXliikbVOLI/AAAAAAAABvc/nIGGb-MnHXk/s1600/Einhovens+Triangle+-+LA-LL+Swap.jpg" imageanchor="1" style="margin-left: auto; margin-right: auto;"><img border="0" src="https://lh5.googleusercontent.com/-9O6oQ8w9CAU/TXliikbVOLI/AAAAAAAABvc/nIGGb-MnHXk/s1600/Einhovens+Triangle+-+LA-LL+Swap.jpg" /></a></td></tr><tr><td class="tr-caption" style="text-align: center;"><b>LA/LL Swap: Einthoven's Triangle is "Flipped"</b></td></tr></tbody></table>We can see that Lead I is actually looking at Lead II and Lead II is actually looking at Lead I; confirmed with ECG's 1 and 2. Lead III becomes an inverted Lead III; confirmed again in the original ECG's.&nbsp;<b>This looks like a case of an unrecognized left arm and left leg lead reversal.</b><br /><br />What I find most interesting is if you compare every ECG except the first, it appears to be a case with subtle posteriolateral changes that may have been missed had there not been the lead reversal!Christopherhttp://www.blogger.com/profile/11415988855392944633noreply@blogger.com0tag:blogger.com,1999:blog-8723582074539021948.post-43010534314345927622011-02-28T19:06:00.001-05:002011-11-22T02:21:32.542-05:00Highlighting Atrial Activity on an ECG: The S5 LeadKelly Grayson, of <a href="http://ambulancedriverfiles.com/">A Day in the Life of an Ambulance Driver</a> fame, posted <a href="http://www.ems1.com/ems-products/technology/articles/746439-The-Leads-Less-Traveled/">an article on EMS1.com over a year ago entitled The Leads Less Traveled</a>. In this he touched on modified chest leads (MCL1 through MCL6), right precordial leads (V4R), and the S5 Lead.<br /><br /><i>Update: after posting this I have since learned it is also known as the <b>Lewis Lead</b>, after Sir Thomas Lewis<sup>1</sup>, and have included a link to an article detailing how it was derived.</i><br /><br />I had never heard of the <b>S5 Lead</b> before and promptly forgot about it until yesterday, when I finished acquiring 12-Leads for my limb lead reversal project. I went ahead and captured a rhythm strip from myself using the S5 lead placement.<br /><table align="center" cellpadding="0" cellspacing="0" class="tr-caption-container" style="margin-left: auto; margin-right: auto; text-align: center;"><tbody><tr><td style="text-align: center;"><a href="https://lh5.googleusercontent.com/-WbEAjkGrYrY/TWw4X-3F7ZI/AAAAAAAABvU/qBN-N0XL8SA/s1600/s5-atrial-leads.jpg" imageanchor="1" style="margin-left: auto; margin-right: auto;"><img border="0" height="92" src="https://lh5.googleusercontent.com/-WbEAjkGrYrY/TWw4X-3F7ZI/AAAAAAAABvU/qBN-N0XL8SA/s400/s5-atrial-leads.jpg" width="400" /></a></td></tr><tr><td class="tr-caption" style="text-align: center;"><b>S5 Leads: monitoring Leads I and II.</b></td></tr></tbody></table><div class="separator" style="clear: both; text-align: center;"></div>Before we cover the S5 Leads, let's recap normal lead placement and our friend, Einthoven's Triangle. This produces convenient ECGs with positive waveforms along the usual mean vector of the heart. Lead I points to 0°, Lead II points to 60°, and Lead III points to 120°.<br /><table align="center" cellpadding="0" cellspacing="0" class="tr-caption-container" style="margin-left: auto; margin-right: auto; text-align: center;"><tbody><tr><td style="text-align: center;"><a href="https://lh3.googleusercontent.com/-p-igMwnR-3E/TWwxcYOBJQI/AAAAAAAABu8/S-Kmrc1dLQM/s1600/normal-vectors.jpg" imageanchor="1" style="margin-left: auto; margin-right: auto;"><img border="0" src="https://lh3.googleusercontent.com/-p-igMwnR-3E/TWwxcYOBJQI/AAAAAAAABu8/S-Kmrc1dLQM/s1600/normal-vectors.jpg" /></a></td></tr><tr><td class="tr-caption" style="text-align: center;"><b>Our friend, Einthoven's Triangle.</b></td></tr></tbody></table>Additionally, the electrodes themselves are placed out on the limbs which generally results in waveforms proportional to the myocardium involved. Atrial activity is shown as well, but considering the proportion of myocardium involved in atrial depolarization, this configuration is not always useful in finding P-waves.<br /><table align="center" cellpadding="0" cellspacing="0" class="tr-caption-container" style="margin-left: auto; margin-right: auto; text-align: center;"><tbody><tr><td style="text-align: center;"><a href="https://lh6.googleusercontent.com/-tHO_12NNdRU/TWwzcFC59hI/AAAAAAAABvE/7-_Ut2k2yg0/s1600/normal-lead-I-II.jpg" imageanchor="1" style="margin-left: auto; margin-right: auto;"><img border="0" src="https://lh6.googleusercontent.com/-tHO_12NNdRU/TWwzcFC59hI/AAAAAAAABvE/7-_Ut2k2yg0/s1600/normal-lead-I-II.jpg" /></a></td></tr><tr><td class="tr-caption" style="text-align: center;"><b>Normal Placement: Leads I and II from the same patient.</b></td></tr></tbody></table>Now let's introduce the <b>S5 Lead</b>. You can produce this using many variations of the electrodes, however, for simplicity's sake we will stick with Kelly's description:<br /><ol><li>Place the <i style="font-weight: bold;">Right Arm </i>electrode on the patient's <u>manubrium</u>.</li><li>Place the <i style="font-weight: bold;">Left Arm</i>&nbsp;electrode on the <u>5th intercostal space,&nbsp;right sternal border</u>.</li><li>Place the <i style="font-weight: bold;">Left Leg</i>&nbsp;electrode on the <u>right lower costal margin</u>.</li><li><b><i>Monitor Lead I</i></b>.</li></ol><table align="center" cellpadding="0" cellspacing="0" class="tr-caption-container" style="margin-left: auto; margin-right: auto; text-align: center;"><tbody><tr><td style="text-align: center;"><a href="https://lh4.googleusercontent.com/-fviLOFKMsEo/TWwywF_3joI/AAAAAAAABvA/0hiIz5Wwbjo/s1600/s5-vectors.jpg" imageanchor="1" style="margin-left: auto; margin-right: auto;"><img border="0" src="https://lh4.googleusercontent.com/-fviLOFKMsEo/TWwywF_3joI/AAAAAAAABvA/0hiIz5Wwbjo/s1600/s5-vectors.jpg" /></a></td></tr><tr><td class="tr-caption" style="text-align: center;"><b>Maximal atrial activity monitoring Lead I, S5 Lead configuration.</b></td></tr></tbody></table><div>Notice the change in the direction of each lead. Lead I now points to the usual mean vector of atrial depolarization. Lead II and lead III are nearly perpendicular to the usual mean vector of ventricular depolarization. What does this mean for the electrocardiographer? If you remember that a vector which travels towards a lead is positive and perpendicular to a lead is isoelectric the answer is easy: <b>atrial activity is highlighted</b>, ventricular activity is diminished.&nbsp;</div><table align="center" cellpadding="0" cellspacing="0" class="tr-caption-container" style="margin-left: auto; margin-right: auto; text-align: center;"><tbody><tr><td style="text-align: center;"><a href="https://lh3.googleusercontent.com/-pjbZsPu_IDo/TWw1VkTMrYI/AAAAAAAABvI/3jtOFVRJHoU/s1600/s5-atrial-lead-i.jpg" imageanchor="1" style="margin-left: auto; margin-right: auto;"><img border="0" height="85" src="https://lh3.googleusercontent.com/-pjbZsPu_IDo/TWw1VkTMrYI/AAAAAAAABvI/3jtOFVRJHoU/s320/s5-atrial-lead-i.jpg" width="320" /></a></td></tr><tr><td class="tr-caption" style="text-align: center;"><b>S5: Lead I</b></td></tr></tbody></table><table align="center" cellpadding="0" cellspacing="0" class="tr-caption-container" style="margin-left: auto; margin-right: auto; text-align: center;"><tbody><tr><td style="text-align: center;"><a href="https://lh3.googleusercontent.com/-iuQ0520hP3k/TWw1gBhmBZI/AAAAAAAABvM/GSU6hWgAj8Y/s1600/s5-atrial-leads-ii.jpg" imageanchor="1" style="margin-left: auto; margin-right: auto;"><img border="0" height="85" src="https://lh3.googleusercontent.com/-iuQ0520hP3k/TWw1gBhmBZI/AAAAAAAABvM/GSU6hWgAj8Y/s320/s5-atrial-leads-ii.jpg" width="320" /></a></td></tr><tr><td class="tr-caption" style="text-align: center;"><b>S5: Lead II</b></td></tr></tbody></table><div>The new direction Lead I points in is not quite perpendicular to the mean vector and it is also closer to the ventricular depolarization, hence we still have clear ventricular activity. However, the direction and location of Lead I is right in front of the atrial depolarization wavefront, giving clear P-waves. Lead II shows a large P-wave and small, nearly isoelectric ventricular activity.</div><div><br /></div><div>If I can remember, I will try and acquire S5 Leads in the field. Has anyone else used the S5 Lead? Are there any other interesting lead configurations we should use?<br /><ol><li>Bakker, ALM, et al. The Lewis Lead: Making Recognition of P Waves Easy During Wide QRS Complex Tachycardia. Circ (2009); 119:e592-e593. [<a href="http://circ.ahajournals.org/content/119/24/e592.full" target="_blank">Free Full Text</a>]</li></ol></div>Christopherhttp://www.blogger.com/profile/11415988855392944633noreply@blogger.com7tag:blogger.com,1999:blog-8723582074539021948.post-68984894927976442782011-02-14T14:46:00.000-05:002011-02-14T14:46:07.419-05:00Limb Lead Reversal: Preliminary FindingsBack in January, <a href="http://ems12lead.com/2011/01/22/the-bait-and-switch/">Tom over at the EMS 12-Lead blog had an interesting case entitled "Bait and Switch"</a> in which the diagnosis of a STEMI was potentially masked due to incorrect limb lead placement. Interestingly, the limb lead placement was not one of classic LA/RA reversal, but rather a "rotation" of the limb leads. In this instance, the cardiac monitor did not detect the incorrect limb lead positioning. Over the last few weeks I have set out to collect 12-Lead ECGs acquired from each of the 24 possible limb lead positions and to catalog the characteristics of each.<br /><br />All of the ECGs I have acquired are on LifePak 12 monitors using the GE Marquette 12SL algorithm. Currently, only classic limb lead reversal has produced the, "*** Suspect arm lead reversal, interpretation assumes no reversal," message. However, I still have 12 combinations of lead placements to complete.<br /><br />Here are 3 ECG's acquired from a healthy male subject without any known cardiac abnormality or history (i.e. me).<br /><br /><table align="center" cellpadding="0" cellspacing="0" class="tr-caption-container" style="margin-left: auto; margin-right: auto; text-align: center;"><tbody><tr><td style="text-align: center;"><a href="http://4.bp.blogspot.com/-fAp45oItz78/TVmEXfAP-RI/AAAAAAAABuc/uuBKgnAsWto/s1600/limb-leads-1248.jpg" imageanchor="1" style="margin-left: auto; margin-right: auto;"><img border="0" height="310" src="http://4.bp.blogspot.com/-fAp45oItz78/TVmEXfAP-RI/AAAAAAAABuc/uuBKgnAsWto/s400/limb-leads-1248.jpg" width="400" /></a></td></tr><tr><td class="tr-caption" style="text-align: center;">Normal ECG **Unconfirmed**; Normal Sinus Rhythm</td></tr></tbody></table><table align="center" cellpadding="0" cellspacing="0" class="tr-caption-container" style="margin-left: auto; margin-right: auto; text-align: center;"><tbody><tr><td style="text-align: center;"><a href="http://3.bp.blogspot.com/-PsBBIC9XvNk/TVmEeFydhXI/AAAAAAAABug/T-2Fn7qgf_A/s1600/limb-leads-2148.jpg" imageanchor="1" style="margin-left: auto; margin-right: auto;"><img border="0" height="311" src="http://3.bp.blogspot.com/-PsBBIC9XvNk/TVmEeFydhXI/AAAAAAAABug/T-2Fn7qgf_A/s400/limb-leads-2148.jpg" width="400" /></a></td></tr><tr><td class="tr-caption" style="text-align: center;">Abnormal ECG **Unconfirmed**; *** Suspect arm lead reversal, interpretation assumes no reversal; Normal sinus rhythm; Right axis deviation; Nonspecific ST abnormality.</td></tr></tbody></table><table align="center" cellpadding="0" cellspacing="0" class="tr-caption-container" style="margin-left: auto; margin-right: auto; text-align: center;"><tbody><tr><td style="text-align: center;"><a href="http://3.bp.blogspot.com/-RpXxRqQxpv0/TVmEkl2n24I/AAAAAAAABuk/UfIxNTiaTAg/s1600/limb-leads-8142.jpg" imageanchor="1" style="margin-left: auto; margin-right: auto;"><img border="0" height="310" src="http://3.bp.blogspot.com/-RpXxRqQxpv0/TVmEkl2n24I/AAAAAAAABuk/UfIxNTiaTAg/s400/limb-leads-8142.jpg" width="400" /></a></td></tr><tr><td class="tr-caption" style="text-align: center;">Abnormal ECG **Unconfirmed**; Unusual P-axis, possible ectopic atrial rhythm; Left axis deviation; ST &amp; T wave abnormality, consider inferior ischemia</td></tr></tbody></table>Christopherhttp://www.blogger.com/profile/11415988855392944633noreply@blogger.com2tag:blogger.com,1999:blog-8723582074539021948.post-14030050286474550962010-12-21T10:52:00.001-05:002010-12-21T10:56:17.905-05:00Harvard's ECG Wave MavenI am constantly searching for resources which let me hone my electrocardiography skills and would like to share a gem I discovered a few months ago. Harvard's School of Medicine and the Beth Israel Deaconess Medical Center has an excellent resource:<a href="http://ecg.bidmc.harvard.edu/maven/mavenmain.asp">&nbsp;ECG Wave Maven: Self-Assessment Program for Students and Clinicians</a>. You can browse their cases as a quiz or for reference, and each case includes high resolution ECGs for your inspection.<br /><br />I've found their difficulty ratings to be pretty accurate, and I've found that Level 3 or less (of 5 difficulty levels) are all ECG findings that Paramedics should be able to recognize.<br /><br /><table align="center" cellpadding="0" cellspacing="0" class="tr-caption-container" style="margin-left: auto; margin-right: auto; text-align: center;"><tbody><tr><td style="text-align: center;"><a href="http://ecg.bidmc.harvard.edu/mavendata/images/case164/800x400.gif" imageanchor="1" style="margin-left: auto; margin-right: auto;"><img border="0" height="200" src="http://ecg.bidmc.harvard.edu/mavendata/images/case164/800x400.gif" width="400" /></a></td></tr><tr><td class="tr-caption" style="text-align: center;"><span class="Apple-style-span" style="font-family: arial; font-size: 11px; line-height: 13px;">Nathanson L A, McClennen S, Safran C, Goldberger AL. ECG Wave-Maven: Self-Assessment Program for Students and Clinicians. <a href="http://ecg.bidmc.harvard.edu/">http://ecg.bidmc.harvard.edu</a>.</span></td></tr></tbody></table>I encourage all of you to go spend&nbsp;a few <s>hours</s>days at the site brushing up on your ECG interpretation skills, your patients deserve it!Christopherhttp://www.blogger.com/profile/11415988855392944633noreply@blogger.com0tag:blogger.com,1999:blog-8723582074539021948.post-75332627067879746932010-12-20T17:08:00.000-05:002010-12-20T17:08:50.116-05:00A quick look at Pulmonary EmbolismsAcute pulmonary embolism (PE) is believed to affect anywhere from 1 in 250 to 1 in 1000 persons in the US each year. Potentially 1 in 10 patients with an acute pulmonary embolism may go into cardiac arrest within the first 60 minutes[1].<br /><br />The working diagnosis of a PE in the field is likely to be based solely on clinical findings. Therefore, prehospital providers should be familiar with the most common physical findings:<br /><ol><li>Tachycardia</li><li>Tachypnea</li><li>Dyspnea</li><li>Persistently low SaO2</li><li>Recent history of syncope</li><li>Hypotension</li><li>Cyanosis or pallor </li><li>Diaphoresis</li><li>Hemoptysis</li><li>Low grade fever</li><li>Diminished lung sounds</li></ol>Additionally, prehospital providers should be familiar with the common ECG findings in acute pulmonary embolisms (in order of prevalence):<br /><ol><li>Sinus tachycardia (73%)</li><li>Prominent S1 (73%) </li><li>"Clock-wise" rotation (56%) </li><li>Negative T in 2+ precordials (50%)</li><li>Incomplete or complete RBBB (20-68%)</li><li>P-pulmonale (28-33%)</li><li>Axis shift, generally RAD (23-30%)</li><li><b>No significant findings (20-24%)</b></li><li>S1Q3T3 (12-25%)</li><li>Supraventricular arrhythmias (12%)</li></ol>Note that 1 in 5 patients are likely to have no significant ECG findings. What this should stress is the field diagnosis of a PE will lean heavily on your clinical assessment and findings. <b>Chou</b>[2] notes that in one study only 5 patients of 64 were diagnosed with a PE based on ECG findings.<br /><br />A combination of any of these physical and electrocardiographic findings strongly favor PE and prehospital providers should act accordingly. Unrecognized pulmonary embolisms may be rapidly fatal.<br /><br /><b>References</b><br /><ol><li>Galvagno SM. Emergency Pathophysiology: Clinical Applications for Prehospital Care. Teton New Media (2003). [<a href="http://www.google.com/search?q=1591610079">ISBN 1591610079</a>]</li><li>Surawics B, Knilans TK, Chou TC. Chou's Electrocardiography in Clinical Practice: Adult and Pediatric. Saunders/Elsevier (2008), 6th ed. [<a href="http://www.google.com/search?q=1416037748">ISBN 1416037748</a>]</li></ol>Christopherhttp://www.blogger.com/profile/11415988855392944633noreply@blogger.com0tag:blogger.com,1999:blog-8723582074539021948.post-42023322062594765342010-12-03T13:49:00.000-05:002010-12-03T13:49:25.375-05:00Pediatric Intranasal Fentanyl<b><span class="Apple-style-span" style="font-size: large;">Scenario</span></b><br />It's a summer afternoon and you're dispatched to a 9 year old male patient involved in an ATV accident. The nearest ALS engine company has been dispatched as well. Upon your arrival you find an ATV on its side, another ATV upright, and a crowd gathered on the porch of a nearby house. A paramedic from the engine is assessing a distraught young boy, sitting in his mother's lap, holding an obviously deformed right forearm. The officer on the engine informs you that the boy and his father were riding alongside the road, traveling at 20-30 miles per hour, when the boy lost control and was thrown from the ATV (his father insists he was wearing his helmet).<br /><br />You introduce yourself to the child, assuring him you're here to help, and ask him what happened. The boy states that when he fell he put his arms out and he heard a loud pop when his right hand hit the ground. He denies passing out or any other injuries but says his arm, "really hurts". He reluctantly allows you to assess his radial pulse in the affected arm, which is rapid but easily palpable.&nbsp;There appears to be distal involvement of both the radius and ulna, however&nbsp;he does not tolerate any further assessment of the arm and screams if there is any movement. The remainder of your physical exam reveals only minor abrasions to exposed skin. The engine company reports tachypnea, tachycardia, and a normal blood pressure.<br /><br /><b><span class="Apple-style-span" style="font-size: large;">Discussion</span></b><br />It appears the child has suffered a Colles' Fracture of the right distal forearm. Appropriate treatment would include splinting, ice packs, and pharmacologic pain control. However, given the current state of the patient, it may not be possible to splint the extremity due to anxiety and pain. Traditional prehospital pain management would require intravenous access or intramuscular administration. Both of these routes are likely to cause increased anxiety in this patient, which is best avoided.<br /><br />Pain management in the pre-hospital setting is fraught with problems. Most studies have found poor provider perception of pain, underutilization of analgesics, and a hesitance to treat pediatric pain (<b>Thomas</b>; <b>Greenwald</b>). Often&nbsp;times, studies find that even if patients are provided analgesia, they do not feel their pain was managed adequately at all (<b>Thomas</b>). For pediatric patients, this problem is compounded as pre-hospital providers are often wary to provide pain management or may be unable to obtain invasive IV access to provide pain management (<b>Greenwald</b>). Moreover, pre-hospital providers are often placed in situations where access to patients is limited to provide pain-management, often times resulting in painful patient movements.<br /><br />The addition of a noninvasive means of pain management would be an invaluable aid to pre-hospital providers and would remove a potential barrier to care. In pediatric populations, the importance of noninvasive pain management procedures is easy to grasp, as this patient population is often unable to comprehend the benefits of initially painful procedures. Improvements in "time to analgesia" will likely lead to and have a direct, positive impact on patient care and satisfaction.<br /><br /><b><span class="Apple-style-span" style="font-size: large;">Efficacy and Safety of Intranasal Fentanyl</span></b><br />The efficacy and safety of intranasal fentanyl (INF) has been the focus of multiple studies, both in-hospital and pre-hospital. <b>Finn et al</b> conducted an in-hospital randomized double-blind placebo controlled trial and found INF to have the same efficacy as oral morphine during procedural wound care in adult burn patients (n=26, 35.5 ± 12.4 years). The concentration of INF used in this study was 50 µg/mL, initial dosages of 1.48 ± 0.57 µg/kg, and no difference in the number of adverse events. <b>Finn et al</b> concluded that while patients receiving INF were more satisfied with their level of pain relief (p = 0.009) that overall only half of the patients in the trial reported they were "satisfied" or "very satisfied".<br /><br />In a randomized, controlled, open-label study of pre-hospital INF versus IV morphine, <b>Rickard et al</b> found no significant difference in efficacy or safety (n=258, 42.3 ± 13.7 years). This study differs from Finn et al in that there were a multitude of chief complaints treated due to an "all-comers" design. Moreover, the doses used of INF was significantly higher at 180 µg divided evenly between the nares with up to two repeat dosages of 60 µg. Patients in the INF group received pain medication earlier than in the IV morphine group, likely owing to the simpler route of administration. Adverse effects were noted to occur more frequently in the INF group (relative risk 2.09, 95% CI 0.92-4.78, p = 0.07), however, the <b>Rickard et al</b> was not powered to adequately detect any statistical difference. One incidence of a significant adverse effect required a termination of the INF protocol, but it was unclear from the study if this was related to the treatment or the patient's condition. <b>Rickard et al</b> concluded that given the safety and efficacy of INF, it is a valuable option in patients where intravenous access is "undesirable or impossible".<br /><br /><b>Borland et al 2005</b> and <b>Borland et al 2007</b> were inpatient randomized double-blind crossover studies evaluating the efficacy and safety of INF versus oral or IV morphine, respectively, in pediatric patients. <b>Borland et al 2005</b> studied INF in pediatric burn patients requiring daily dressing changes and found no significant difference in outcomes (n=24, median 4.5 IQR 1.8-9.0 years). The INF dosage was calculated against the bioavailability of the IN route (listed as 70%) with 1.4 µg/kg fentanyl equating to an IV dosage of 1 µg/kg. There were no incidents of significant adverse events, although this was likely due to the study size. However, sedation scores recorded found that INF patients recovered earlier than their oral morphine counterparts. Overall, <b>Borland et al 2005</b> found INF to be safe and efficacious, but more importantly well tolerated by pediatric patients.<br /><br /><b>Borland et al 2007</b> found INF to be comparable to intravenous morphine in pediatric patients presenting to the emergency department with acute long-bone fractures (n=67, 10.9 ± 2.4 years). The median total dose was 1.7 µg/kg fentanyl with repeat doses given PRN. The impetus of the study was to find alternative methods of analgesia to intravenous narcotics in the pediatric population. The study authors note that given the comparable efficacy, INF is invaluable as a means to decrease "time to analgesia" in the pediatric population with potential for pre-hospital adoption.<br /><br /><b>Mudd</b> conducted a systematic review of the available literature for INF in the pediatric population and graded 12 studies with evidence qualities of four Level I/A, one II/A, two II/B, one III/A, and four at III/B. There was a wide variation in dosing of INF amongst the studies, with a common range of 1-2 µg/kg fentanyl. Differences in concentrations existed as well, owing to the fact that in the US fentanyl is commonly available at 50 µg/mL and is used IV/IM/IO/IN yet overseas it is often given IN with a more concentrated 100-150 µg/mL solution. No differences in significance in pain reduction were found between concentrations, only in the volume of medication delivered. While no studies found a significant difference in adverse effects, many studies had small sample sizes and no long-term studies have been completed on the action of fentanyl on the nasal mucosa. However, the evidence in the reviewed studies demonstrated three clear points: (1) that INF is as efficacious as IV/IM/PO morphine or IV fentanyl, (2) it has no difference in adverse effects, and (3) it decreases the time to analgesia administration and pain relief.<br /><br /><b><span class="Apple-style-span" style="font-size: large;">Intranasal Fentanyl Protocol</span></b><br />Based on the research available and the existing <a href="http://www.ncems.org/nccep.html">2009 NC EMS protocols</a>, an appropriate pain management protocol for the administration of intranasal fentanyl is given below:<br /><ul><li>Adult patients with indications for narcotic analgesia for whom intravenous access is not feasible, not available, or at the discretion of the lead Paramedic, an initial dose of 50-75 µg fentanyl may be delivered intranasally. The total volume to be administered should be divided equally between the two nares (not to exceed 1mL per nare).<br /><ul><li>If intravenous access is not available, repeat with 25 µg fentanyl delivered intranasally every 20 minutes to a maximum total dose of 200 µg.</li></ul></li><li>Pediatric patients with indications for narcotic analgesia an initial dose of 1-2 µg/kg fentanyl up to a total dose of 50 µg may be delivered intranasally. The total volume to be administered should be divided equally between the two nares (not to exceed 0.5mL per nare).<br /><ul><li>In order to decrease the anxiety of pediatric patients requiring analgesia and invasive procedures (such as intravenous access), it may be prudent to begin with intranasal fentanyl.</li></ul></li></ul><b><span class="Apple-style-span" style="font-size: x-small;">References</span></b><br /><ul><li><span class="Apple-style-span" style="font-size: x-small;">M. Borland, I. Jacobs and I. Rogers, Options in prehospital analgesia, <i>Emerg Med</i> (Freemantle) <b>14 </b>(2002), pp. 77–84.</span></li><li><span class="Apple-style-span" style="font-size: x-small;">M. Borland, I. Jacobs and G. Geelhoed, Intranasal fentanyl reduces acute pain in children in the emergency&nbsp;department: a safety and efficacy study, <i>Emerg Med</i> (Freemantle) <b>14 </b>(2002), pp. 275–280.</span></li><li><span class="Apple-style-span" style="font-size: x-small;">J. Finn, J. Wright, J. Fong, E. Mackenzie, F. Wood, G. Leslie and A. Gelavis, A randomized crossover trial of patient&nbsp;controlled intranasal fentanyl and oral morphine for procedural wound care in adult patients with burns, <i>Burns&nbsp;</i><b>30 </b>(3) (2004), pp. 262–268.</span></li><li><span class="Apple-style-span" style="font-size: x-small;">M. Borland, R. Bergesio and E.M. Pascoe et al., Intranasal fentanyl is an equivalent analgesic to oral morphine in&nbsp;paediatric burns patients for dressing changes: a randomised double blind crossover study, <i>Burns </i><b>31 </b>(2005), pp.&nbsp;831–837.</span></li><li><span class="Apple-style-span" style="font-size: x-small;">M. Borland, I. Jacob and B. King et al., A randomized controlled trial comparing intranasal fentanyl to&nbsp;intravenous morphine for managing acute pain in the emergency department, <i>Ann Emerg Med</i> <b>49 </b>(2007), pp.&nbsp;335–340.</span></li><li><span class="Apple-style-span" style="font-size: x-small;">C. Rickard, P. O’Meara, M. McGrail, et al., A randomized controlled trial of intranasal fentanyl vs intravenous&nbsp;morphine for analgesia in the prehospital setting, <i>Amer J Emerg Med</i> <b>25 </b>(2007), pp. 911-917.</span></li><li><span class="Apple-style-span" style="font-size: x-small;">S. Thomas, S. Shewakramani, Prehospital Trauma Analgesia, <i>J Emerg Med</i> <b>35 </b>(2007), pp. 47-57.</span></li><li><span class="Apple-style-span" style="font-size: x-small;">M. Greenwald, Analgesia for the Pediatric Trauma Patient: Primum Non Nocere? <i>Clin Pedi Emerg Med</i> <b>11 </b>(2010),&nbsp;pp. 28-40.</span></li><li><span class="Apple-style-span" style="font-size: x-small;">S. Mudd, Intranasal Fentanyl for Pain Management in Pediatrics: A Review of the Literature, <i>J Pedi Health Care</i>&nbsp;(2010), Article in Press. <a href="http://www.jpedhc.org/article/S0891-5245(10)00098-2/fulltext">doi:10.1016/j.pedhc.2010.04.011</a>.</span></li></ul>Christopherhttp://www.blogger.com/profile/11415988855392944633noreply@blogger.com0tag:blogger.com,1999:blog-8723582074539021948.post-90136752256983655522010-10-22T18:33:00.000-04:002010-10-22T18:33:46.810-04:00One Year: Thank YouOne year has passed since I received my EMT-Paramedic, and I'd like to say thank you.<br /><br />Firstly, to my friends and family. You have endured my absence well, or at least have hid your anger well. I'm sure this last year has been tough, but probably not as tough as paramedic school. I really could not do this job without your support, especially as a volunteer. I cannot say it enough, thank you.<br /><br />To my colleagues and peers, you have surely challenged me to accomplish things I never knew I was capable of doing. You have mentored me, scolded me, and sat patiently while I fumbled with IVs. There is an entire network of you online which have been invaluable as a sounding board and a reference. I can only hope I will continue to take what you have given me and make myself a better Paramedic going forward. The fact that I feel like my feet are underneath me at all is a testament to you all, thank you.<br /><br />Lastly, to my patients of whom I've met quite a few: you have taught me more than I could ever hope to tell you.&nbsp;Some of you were thrust into my arms, others I knelt and said goodbye.&nbsp;You have challenged me to better myself and I appreciate every experience.&nbsp;My life as a green Paramedic has been an odd mix of on-the-job training for emergencies I was never told about and connecting the dots for those I was told every day about. I thank you for your understanding.&nbsp;I hope that I can tell a story of that time I sat next to you on a flight, and heard about your trip to see your&nbsp;niece&nbsp;get married. That is why I am here, you are why I am here. I feel blessed to meet each and every one of you, thank you.Christopherhttp://www.blogger.com/profile/11415988855392944633noreply@blogger.com1tag:blogger.com,1999:blog-8723582074539021948.post-13050609793785981912010-10-18T15:30:00.001-04:002010-10-18T16:32:26.186-04:002010 AHA CPR/ECC GuidelinesIf you haven't already heard, today the <a href="http://circ.ahajournals.org/content/vol122/18_suppl_3/">AHA released the 2010 edition of their CPR/ECC Guidelines</a> which include updates for laypersons, BLS, ACLS, PALS, and neonatal resuscitation. If you've been following resuscitation research at all for the last few years, there are not many surprises.<br /><br /><ol><li>Compressions trump ventilations in adult patients (<b>C-A-B</b> not A-B-C).</li><li>Minimize interruptions in the "flow" of a resuscitation, that is, continuous compressions are to be minimally interrupted.</li><li>ETCO2 is to be preferred over manual pulse checks: if you don't have a rise in ETCO2 to physiologic or near-physiologic levels, you probably do not have a perfusing rhythm.</li><li>AEDs are indicated for all ages, including infants and neonates, provided there are pads available which fit without overlap (&gt;3cm gap).</li><li>Pharmacologic therapy has the same weight as TCP in certain bradyarrhythmias.</li><li>Procainamide is now first-line or at least recommended on par with Amiodarone, Lidocaine is almost off the list.</li><li>Atropine is no longer recommended during routine PEA/Asystole resuscitations.</li><li>Studies into neonatal resuscitation have shown that deep suctioning is not required in vigorously born neonates with meconium staining.</li><li>Routine use of naloxone in cardiac arrest secondary to opioid overdose is not recommended.</li></ol><div>There were many other differences, including the addition of circular flowcharts documenting the new guidelines (linear flowcharts are still provided). I encourage everyone to read them.<br /><br /><b>Edit:</b>&nbsp;here is a <a href="http://www.heart.org/idc/groups/heart-public/@wcm/@ecc/documents/downloadable/ucm_317350.pdf">document (PDF) comparing the AHA 2005 CPR/ECC guidelines to the 2010 guidelines</a>.</div>Christopherhttp://www.blogger.com/profile/11415988855392944633noreply@blogger.com0tag:blogger.com,1999:blog-8723582074539021948.post-72232594399071093992010-09-13T16:59:00.001-04:002010-09-13T17:04:01.426-04:00How many Automated External Defibrillators are at your place of work?<span class="Apple-style-span" style="font-family: Arial; font-size: small;"><span class="Apple-style-span" style="font-size: 13px;">Our Industrial Fire Brigade just added 10 more AEDs to our site. By my rough calculations this means we have 1 AED for every 150 employees and 1 AED for every 80,000 sqft of floor space (we have almost 2 million sqft). To put this in perspective, the recommendations generally are for 1 AED per 100,000-150,000 sqft or building floor. We now have an AED and emergency responders within 2 minutes of every employee on site!</span></span><br /><div><span class="Apple-style-span" style="font-family: Arial; font-size: small;"><span class="Apple-style-span" style="font-size: 13px;"><br /></span></span></div><table align="center" cellpadding="0" cellspacing="0" class="tr-caption-container" style="margin-left: auto; margin-right: auto; text-align: center;"><tbody><tr><td style="text-align: center;"><a href="http://4.bp.blogspot.com/_XnHVrPnrx7o/TI6P9Ffzv1I/AAAAAAAABss/ALrpbaGpp3A/s1600/heartstarts.jpg" imageanchor="1" style="margin-left: auto; margin-right: auto;"><img border="0" height="295" src="http://4.bp.blogspot.com/_XnHVrPnrx7o/TI6P9Ffzv1I/AAAAAAAABss/ALrpbaGpp3A/s400/heartstarts.jpg" width="400" /></a></td></tr><tr><td class="tr-caption" style="text-align: center;">The Philips HeartStart FRx is a great first responder AED as this author has learned through personal experience.</td></tr></tbody></table><div><span class="Apple-style-span" style="font-family: Arial; font-size: small;"><span class="Apple-style-span" style="font-size: 13px;">How does your place of work stack up? Do you need help with corporate/management buy-in? Perhaps our site's successes can help you out. Let me know!</span></span></div>Christopherhttp://www.blogger.com/profile/11415988855392944633noreply@blogger.com0tag:blogger.com,1999:blog-8723582074539021948.post-91579906277207650862010-09-07T14:59:00.002-04:002010-09-16T22:17:25.674-04:0012-Lead ECG: What Is It?While cleaning up my office to put in a reading chair, I found the following 12-Lead ECGs from my clinical time. &nbsp;I apologize for the poor quality of the first one, but it is a copy of a copy (of probably a copy). I have limited information on the patients for each of them somewhere in my clinical binder, but I haven't found those yet.<br /><table align="center" cellpadding="0" cellspacing="0" class="tr-caption-container" style="margin-left: auto; margin-right: auto; text-align: center;"><tbody><tr><td style="text-align: center;"><a href="http://3.bp.blogspot.com/_XnHVrPnrx7o/TIaLbF_yv6I/AAAAAAAABsc/YNxSl0ygrFk/s1600/ECG+What+Is+It+1.jpg" imageanchor="1" style="margin-left: auto; margin-right: auto;"><img border="0" height="308" src="http://3.bp.blogspot.com/_XnHVrPnrx7o/TIaLbF_yv6I/AAAAAAAABsc/YNxSl0ygrFk/s400/ECG+What+Is+It+1.jpg" width="400" /></a></td></tr><tr><td class="tr-caption" style="text-align: center;"><b>ECG 1</b></td></tr></tbody></table><br /><table align="center" cellpadding="0" cellspacing="0" class="tr-caption-container" style="margin-left: auto; margin-right: auto; text-align: center;"><tbody><tr><td style="text-align: center;"><a href="http://1.bp.blogspot.com/_XnHVrPnrx7o/TIaLH9jN83I/AAAAAAAABsU/FJTRGAyxbgQ/s1600/ECG+What+Is+It+3.jpg" imageanchor="1" style="margin-left: auto; margin-right: auto;"><img border="0" height="308" src="http://1.bp.blogspot.com/_XnHVrPnrx7o/TIaLH9jN83I/AAAAAAAABsU/FJTRGAyxbgQ/s400/ECG+What+Is+It+3.jpg" width="400" /></a></td></tr><tr><td class="tr-caption" style="text-align: center;"><b>ECG 2</b></td></tr></tbody></table><br /><div style="margin: 0px;">What do these two 12-Leads show?</div><div style="margin: 0px;"><br /></div><div style="margin: 0px;">Do you agree with the computerized statements?<br /><br /><b>Update on ECG 1</b> (16 Sept 2010)<br /><b><br /></b><br />The patient's lab values include a K+ of 2.1 mEq/L. What are some of the expected ECG changes in hypokalemia? Does this ECG show a classical or atypical presentation of hypokalemia?</div>Christopherhttp://www.blogger.com/profile/11415988855392944633noreply@blogger.com5tag:blogger.com,1999:blog-8723582074539021948.post-32244116313721882732010-08-23T17:28:00.004-04:002010-09-03T14:30:50.193-04:00Pediatric Transcutaneous PacingBeing out of school only recently, I'm often asked "book" questions which are likely to be fresh in my mind. One of these that had me stumped was simply, "<b>what is the appropriate current settings for pediatric transcutaneous pacing?</b>"<br /><br />I had no answer.<br /><br />Honestly I had no idea, but assumed it would be weight based, and along the lines of the PALS guidelines for defibrillation. However, when I researched this topic in my PALS book I found there were no answers for pediatric pacing [<a href="#pace_ref1">1</a>]. In fact, there was little mention of TCP whatsoever! Going over to ACLS I found no answers for current settings in adults, just when it was indicated [<a href="#pace_ref2">2</a>].<br /><br />However, in Paramedic school we had been taught the appropriate current ranges for TCP in adults, which ranged from 20-200 mA. <b>Zoll et al</b> found that most adults responded to TCP in the range of 40-70 mA, however, some required currents up to the device maximum of 140 mA [<a href="#pace_ref3">3</a>]. After a few hours of searching for guidelines specific to pediatrics (including the Philips, Physio-Control, and Zoll websites), I came across a study on TCP in pediatrics which focused on the current required for different electrode sizes. Much to my amazement, <b>the current settings required for external transcutaneous pacing of pediatrics are the same as for an adult</b>!<br /><blockquote>A total of 56 pacing trials were conducted, 53 of which were successful in obtaining capture. A mean output of 63 +/- 14 mA (range, 42-98) at threshold using the large electrodes was comparable to published adult requirements. <b>Béland MJ et al</b> [<a href="#pace_ref4">4</a>]</blockquote>How could this be, <b>wouldn't a smaller heart need less energy</b>?<br /><br />It seemed paradoxical at first, but reviewing the anatomy and physiology of a myocyte with an emphasis on the physics aspect puts it into perspective [<a href="#pace_ref5">5</a>]. Each myocyte in the heart is a part of what amounts to an big electromechanical pump. Given a sufficient input stimulus a myocyte contracts and forwards a stimulus to its neighbors, which follow suit, leading to the eventual coordination of systole and diastole.<br /><br />The goal of any artificial cardiac pacemaker, whether internal or external, is to act as the primary input stimulus by applying a current to an area of the heart which exceeds the <i>stimulation threshold</i>, i.e. the current required to cause a response from the myocardium. <br /><br />Therefore, transcutaneous cardiac pacemakers attempt to exceed the stimulation threshold&nbsp;<b>of a single area</b>. It would be hard to achieve coordinated ventricular activity if the current was too high, instead you would have defibrillation. It stands to reason that if the only threshold required to overcome is the stimulation threshold of a single area of the myocardium, the weight of the heart--generalized as the weight of the patient--would be irrelevant.<br /><br />In contrast, the goal of defibrillation is to bring all electrical activity in the heart to a halt. Defibrillation is not successful unless the all of the reentrant activations of ventricular fibrillation are stopped. Therefore the therapeutic energy levels are going to be proportional to the amount of myocardium you are acting on. Hence, pediatric defibrillation energy dosages are weight based.<br /><br />So what seemed counterintuitive at first, is actually fairly logical. Pediatric transcutaneous cardiac pacing has the same energy requirements as adults because myocardium has the same stimulation threshold regardless of age. This deduction is supported in the literature as well:<br /><blockquote>No correlation has been defined between transcutaneous pacing threshholds and age, body weight, body surface area, chest diameter, cardiac drug therapy, or etiology of underlying heart disease. [<a href="#pace_ref6">6</a>]</blockquote>So there we have it, transcutaneous cardiac pacing current setting ranges are universal amongst our patient population. Below is a guideline I've created as a supplement to the material contained within PALS:<br /><blockquote><b>Pediatric Transcutaneous Cardiac Pacing</b><br />Symptomatic bradycardia in the pediatric population is most often related to hypoxia secondary to respiratory etiologies. In rare situations it may exist in spite of adequate ventilation and oxygenation. Given the presence of a high degree heart blocks, or symptomatic bradycardia refractory to aggressive BLS and ALS treatments, transcutaneous cardiac pacing should be initiated without delay.<br /><br /><b>Indications</b><br /><ul><li>High degree heart blocks</li><li>Symptomatic bradycardia refractory to ventilation, oxygenation, chest compressions, and pharmacological treatments</li></ul><br /><b>Contraindications</b><br />The only contraindication of TCP is an inability to place the pads on the patient without overlap or sufficient distance between them.<br /><br /><b>Side Effects</b><br />The side effects of TCP are most frequently muscle activation and associated pain. These are dose dependent effects which are a combination of the current delivered, size of the pads, location of the pads, and width (time) of the delivered pulse [<a href="#ref7">7</a>].<br /><br />To minimize these side effects use the largest available pads, placing them in an Apical-Posterior fashion. While larger pads require higher current outputs, there is a decrease in the current delivered per surface area reducing the side effects associated with TCP.<br /><br />Often, management of these side effects is achieved through concurrent pharmacological treatment with analgesics and/or sedatives.<br /><br /><b>Dose</b><br />Pediatric transcutaneous cardiac pacing (TCP) is defined by two dosing parameters: output current and rate. This guideline assumes the pacemaker is in fixed mode.<br /><br /><i>Output Current</i><br />As with adult patients, the output current for pediatric transcutaneous cardiac pacing should begin at 20 mA (or the lowest setting available) and increase in 5-10 mA increments until electromechanical capture is obtained. Additionally, the current may be increased an additional 5-10 mA above the determined threshold to ensure continued capture. If the device maximum output current is reached and no electromechanical capture exists, discontinue TCP and troubleshoot. Attempt an alternative pad placement (anterio-apical or anterior-posterior) and ensure the negative pad is on the anterior aspect of the chest. If capture is still not obtained, resume CPR and obtain expert consultation.<br /><br /><i>Output Rate</i><br />In contrast to adult patients, the output rate for pediatric transcutaneous cardiac pacing is age based. The final output rate should be titrated to an adequate systolic blood pressure to resolve perfusion problems, e.g. an improvement in mental status. Care should be taken to avoid tachycardic rates or hypertension. Consult a length-based resuscitation tape (e.g. Broselow™ tape) for appropriate starting output rates and systolic blood pressure. An example table is given below, adapted from the North Carolina 2009 EMS Standards [<a href="#pace_ref8">8</a>]:<br /><br /><table align="center" border="1" style="width: 350px;"><tbody><tr><th>Age</th><th>Rate (bpm)</th><th>Systolic BP (mmHg)</th></tr><tr><td align="center">0-3 mo</td><td align="center">120-150</td><td align="center">85 (+/-25)</td></tr><tr><td align="center">3-6 mo</td><td align="center">120-130</td><td align="center">90 (+/-30)</td></tr><tr><td align="center">7-10 mo</td><td align="center">120</td><td align="center">96 (+/-25)</td></tr><tr><td align="center">11-18 mo</td><td align="center">110-120</td><td align="center">100 (+/-30)</td></tr><tr><td align="center">19-35 mo</td><td align="center">110-120</td><td align="center">100 (+/-20)</td></tr><tr><td align="center">3-4 yr</td><td align="center">100-110</td><td align="center">100 (+/-20)</td></tr><tr><td align="center">5-6 yr</td><td align="center">100</td><td align="center">100 (+/-15)</td></tr><tr><td align="center">7-9 yr</td><td align="center">90-100</td><td align="center">105 (+/-15)</td></tr><tr><td align="center">10-12 yr</td><td align="center">80-90</td><td align="center">115 (+/-20)</td></tr><tr><td align="center">&gt;12 yr</td><td align="center">70-80</td><td align="center">120 (+/-20)</td></tr></tbody></table></blockquote><div><b>References</b><br /><ol><li><a href="" name="pace_ref1">American Heart Association. 2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care: Part 12: Pediatric Advanced Life Support. Circ 2005; 112 (24): [Suppl I:] IV-167-IV-187.</a> [<a href="http://circ.ahajournals.org/cgi/content/full/112/24_suppl/IV-167">Full Text</a>]</li><li><a href="" name="pace_ref2">American Heart Association. 2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care: Part 5: Electrical Therapies. Circ 2005; 112: [Suppl I:] IV-35-IV-46.</a> [<a href="http://circ.ahajournals.org/cgi/content/full/112/24_suppl/IV-35">Full Text</a>]</li><li><a href="" name="pace_ref3">Zoll PM, et al. External noninvasive temporary cardiac pacing: clinical trials. Circ 1985; 71: 937-944.</a> [<a href="http://circ.ahajournals.org/cgi/reprint/71/5/937">Full Text PDF</a>]</li><li><a href="" name="pace_ref4">Béland MJ, et al. Noninvasive transcutaneous cardiac pacing in children. Pacing Clin Electrophysiol. 1987 Nov; 10(6):1262-70.</a> [<a href="http://www.ncbi.nlm.nih.gov/pubmed/2446273">PubMed</a>]</li><li><a href="" name="pace_ref5">Malmivuo J, Plonsey R. Bioelectromagnetism: Principles and Applications of Bioelectric and Biomagnetic Fields. 1985 New York: Oxford University Press. Chaps 15,19,23-24.</a> [<a href="http://www.bem.fi/book/00/tx.htm">Full Text</a>]</li><li><a href="" name="pace_ref6">Ellenbogen KA, Wood MA. Cardiac pacing and ICDs. 2005: Wiley-Blackwell. pp 163-191.</a> [<a href="http://books.google.com/books?id=qchWint-HxgC">Google Books</a>]</li><li><a href="" name="pace_ref7">Bocka JJ. eMedicine: External Pacemakers. 23 Sep 2009. Retrieved 17 Aug 2010.</a> [<a href="http://emedicine.medscape.com/article/780639-overview">Website</a>]</li><li><a href="" name="pace_ref8">2009 NC EMS Standards Document: Color Coded Pediatric Drug List B. Retrieved 17 Aug 2010.</a> [<a href="http://www.ncems.org/pdf/PediatricDrugListB2009.pdf">Full Text PDF</a>]</li></ol></div>Christopherhttp://www.blogger.com/profile/11415988855392944633noreply@blogger.com2tag:blogger.com,1999:blog-8723582074539021948.post-41406303362535999012010-07-28T18:34:00.000-04:002010-07-28T18:34:06.083-04:00Hands-Only CPR<a href="http://blogs.nejm.org/now/index.php/every-breath-you-shouldnt-take/2010/07/28/">Now@NEJM just posted an article detailing the results of two new studies on Hands-Only or Compressions-Only CPR or Cardiocerebral Resuscitation (CCR)</a>. These studies[1,2] look very promising, in fact they showed no appreciable difference in overall survival-to-discharge for traditional CPR versus CCR. Moreover, when one of the studies, by <b>Rea et al</b>[1], compared using CCR to CPR survival-to-discharge of cardiac arrest victims of a primary cardiac etiology there was an increase from 12.3% to 15.5%, although it was not statistically significant. However, when comparing CCR to CPR to non-cardiac etiologies, there was a higher percentage of survivability in the CPR group (7.2% vs. 5.0%), although this as well was not statistically significant.<br /><br /><b>So what does this mean?</b><br /><br />The researchers in <b>Rea et al</b>[1] note that while there was no statistically significant difference between the two, there was a clinically significant trend towards higher survival-to-discharge numbers using compressions alone. Additionally, 80.5% (n=981) of callers given compressions-only instructions began compressions versus 72.7% (n=960) given traditional CPR instructions. Overall 76.7% (n=1941) of callers began either CCR or CPR, which means 1 in 4 callers declined to perform some form of resuscitation.<br /><br />Taking a closer look at the efficacy of the caller instructions, there is a nearly 8% increase in initiation of compressions under compressions-only instructions. Applying that increase to the CPR-instructions group would have meant nearly 75 more patients would have received compressions! Potentially another 9 people could have gone home from the hospital. Rea et al went as far as saying this was a clinically significant difference, but we all know how big of a difference it makes having just one more person walk home.<br /><br /><b>So what should we do?</b><br /><br />I think progressive systems with tight integration between first responders, EMS, and dispatch need to get the Hands-Only word out to the public. Start using Hands-Only dispatch instructions along with an aggressive public information campaign. I feel in just a 60-90 second TV advertisement, Hands-Only CPR could be demonstrated to the public effectively. You could even throw in your favorite prime time TV cast to really capture those eyeballs.<br /><br />I've not been in EMS very long, but my heart sinks every time I walk into a house and there has been no attempt at CPR. Our response times are often in the 8-9 minute range which means most of our attempts are futile. I understand the psychological barriers are high, but we need something to improve the rates of bystander CPR. If these studies have shown one thing, it is that Hands-Only CPR has a good chance of doing just that.<br /><br /><b><span class="Apple-style-span" style="font-size: small;">References</span></b><br /><span class="Apple-style-span" style="font-size: small;">1. Rea TD, et al. CPR with Chest Compression Alone or With Rescue Breathing. N Engl J Med 2010; 363: 423-433. [</span><a href="http://www.nejm.org/doi/full/10.1056/NEJMoa0908993"><span class="Apple-style-span" style="font-size: small;">at nejm.org</span></a><span class="Apple-style-span" style="font-size: small;">]</span><br /><span class="Apple-style-span" style="font-size: small;"><i>Conclusions</i>: Dispatcher instruction consisting of chest compression alone did not increase the survival rate overall, although there was a trend toward better outcomes in key clinical subgroups. The results support a strategy for CPR performed by laypersons that emphasizes chest compression and minimizes the role of rescue breathing.</span><br /><span class="Apple-style-span" style="font-size: small;"><br /></span><br /><span class="Apple-style-span" style="font-size: small;">2. Svensson L, et al. Compression-Only CPR or Standard CPR in Out-of-Hospital Cardiac Arrest. N Engl J Med 2010; 363: 434-442. [</span><a href="http://www.nejm.org/doi/full/10.1056/NEJMoa0908991"><span class="Apple-style-span" style="font-size: small;">at nejm.org</span></a><span class="Apple-style-span" style="font-size: small;">]</span><br /><span class="Apple-style-span" style="font-size: small;"><i>Conclusions</i>:&nbsp;This prospective, randomized study showed no significant difference with respect to survival at 30 days between instructions given by an emergency medical dispatcher, before the arrival of EMS personnel, for compression-only CPR and instructions for standard CPR in patients with suspected, witnessed, out-of-hospital cardiac arrest.</span>Christopherhttp://www.blogger.com/profile/11415988855392944633noreply@blogger.com1tag:blogger.com,1999:blog-8723582074539021948.post-10470923996858549592010-07-20T15:34:00.000-04:002010-07-20T15:34:04.219-04:00Morphine Equivalents VisualizedMy day job involves the creation of visualization software to help engineers evaluate complex systems. In my last post detailing Morphine Equivalents there was math, and numbers, and eyes glazing. So, as an aide to the previous post I submit to you a graph of the three narcotic dosing schedules. I pulled the half-lives from Wikipedia and assumed a bioavailability of 100% for the IV route.<br /><div class="separator" style="clear: both; text-align: center;"></div><div class="separator" style="clear: both; text-align: center;"></div><div class="separator" style="clear: both; text-align: center;"><a href="http://2.bp.blogspot.com/_XnHVrPnrx7o/TEX5-0qrtjI/AAAAAAAABrc/PmdDS4tCC1E/s1600/narcotic+schedules.png" imageanchor="1"><img border="0" src="http://2.bp.blogspot.com/_XnHVrPnrx7o/TEX5-0qrtjI/AAAAAAAABrc/PmdDS4tCC1E/s1600/narcotic+schedules.png" /></a></div><br /><div class="separator" style="clear: both; text-align: center;"></div>The half-lives used are:<br /><ul><li><b>Morphine</b>: 2-3 hours</li><li><b>Fentanyl</b>: 2-4 hours</li><li><b>Dilaudid</b>: 2-3 hours</li></ul>Christopherhttp://www.blogger.com/profile/11415988855392944633noreply@blogger.com1